TOHOKU UNIVERSITY Researchers

Details of the Researcher

Home

日本語 English

Emiko Sato

Section

Graduate School of Pharmaceutical Sciences

Job title

Associate Professor

Degree

博士（医学）（東北大学）
博士（生命科学）（東北大学）
修士（生命科学）（東北大学）

researchmap

https://researchmap.jp/read0145819

J-GLOBAL ID

200901022726785394

Research History 5

2019/12 - Present

Tohoku University　Graduate School of Pharmaceutical Sciences
2011 - Present

Tohoku University Hospital　University Hospital Nephrology, Endocrinology and Vascular Medicine
2011 - 2019/11

Tohoku University　Graduate School of Pharmaceutical Sciences
2009 - 2011

Tohoku University　New Industry Creation Hatchery Center
2004 - 2009

Tohoku University　New Industry Creation Hatchery Center

Education 4

東北大学大学院　生命科学研究科　分子生命科学専攻博士前期課程

2002 - 2004
弘前大学　農学生命科学部　生物機能科学科

1998 - 2002
東北大学大学院　論文博士(医学)取得

2017 -
東北大学大学院　論文博士(生命科学)取得

2007 -

Committee Memberships 2

一般社団法人日本腎臓リハビリテーション学会　代議員

2024/05 - Present
（一社）医用マススペクトル学会　理事

2016/04 - Present

Professional Memberships 6

日本腎臓リハビリテーション学会
THE PHARMACEUTICAL SOCIETY OF JAPAN
日本高血圧学会
JAPANESE SOCIETY OF NEPHROLOGY
JAPANESE SOCIETY FOR BIOMEDICAL MASS SPECTROMETRY
SOCIETY FOR FREE RADICAL RESEARCH JAPAN

︎Show all ︎Show first 5

Research Interests 11

細胞内代謝
尿毒素
胎児発育不全
腎発達
認知機能障害
Oxidative Stress
筋萎縮
Uremic Sarcopenia
Metabolomics
Mass Spectrometory
Chronic Kidney Disease

Research Areas 3

Life sciences / Rehabilitation science /
Life sciences / Nutrition and health science /
Life sciences / Nephrology /

Awards 10

東北大学優秀女性研究者賞「紫千代萩賞」

2025/02　東北大学
Women Researchers Incentice Award

2024/10　The Japanease Society of Hypertension
第19回インテリジェント・コスモス奨励賞

2020/05　「臓器内代謝変化を標的とした慢性腎臓病合併症の予防・治療法の開発」
奨励賞

2017/09　（一社）医用マススペクトル学会　「慢性腎臓病患者においてインドキシル硫酸による骨格筋内代謝変化がウレミックサルコペニアを誘導する」
特別奨励賞

2016/12　腎不全研究会　「骨格筋内への尿毒素蓄積によるサルコペニア発症機序の解明」
学術奨励賞

2016/08　（一社）日本酸化ストレス学会　「筋細胞における尿毒素性酸化ストレスは代謝変化を引き起こしサルコペニアの原因となる」
The excellent poster award

2015/09　International Maillard Reaction Society　「Carbonyl stress and inappropriate renin angiotensin system activity associate with blood pressure elevation」
若手奨励賞

2015/08　グアニジノ化合物研究会　「腹膜透析治療中腎不全患者におけるグアニジノ化合物の意義」
優秀演題賞

2010/06　（一社）日本酸化ストレス学会　「In vitro スーパーオキサイド発生酵素：キサンチンオキシダーゼ・NAD(P)Hオキシダーゼの評価」
優秀演題賞

2008/06

Show all ︎Show 5

Papers 113

Lactoferrin attenuates renal fibrosis and uremic sarcopenia in a mouse model of adenine-induced chronic kidney disease. International-journal

Yukina Iwamoto, Seiko Yamakoshi, Akiyo Sekimoto, Koji Hosomi, Takashi Toyama, Yoshiro Saito, Jun Kunisawa, Nobuyuki Takahashi, Eikan Mishima, Emiko Sato

The Journal of nutritional biochemistry　110039-110039　2025/07/24

DOI： 10.1016/j.jnutbio.2025.110039 　

More details Close

The prevalence of chronic kidney disease (CKD) continues to rise, highlighting the urgent need for effective therapeutic interventions to address its various complications including sarcopenia. Lactoferrin, a multifunctional iron-binding glycoprotein found in mammalian breast milk, exhibits various biological activities and holds potential for treating CKD and its complications. This study investigated the effects of lactoferrin on CKD progression, its complications, and underlying mechanisms. A mouse model of adenine-induced renal failure was used as a CKD model. Lactoferrin was administered during the same period as adenine administration to assess its preventative effect on the progression of CKD. In another experiment, lactoferrin was administered after the adenine administration period to examine its effect on already advanced CKD. Effects of lactoferrin on renal function, renal pathology, and muscle atrophy were evaluated. Additionally, mechanistic insights were explored through mRNA and protein expression profiling, gut microbiota characterization, and metabolomic analysis. Lactoferrin administration improved reduction of renal function, and mitigated renal atrophy, and tubulointerstitial damage, and ameliorated skeletal muscle atrophy in CKD mice. In the skeletal muscle, CKD induced aberrant activation of mTOR1, impaired autophagy, and disrupted branched-chain amino acid metabolism. These abnormal activation of the proteolysis pathways was ameliorated by lactoferrin. Furthermore, lactoferrin attenuated dysbiosis-induced production of microbiota-derived uremic toxins, thereby reducing the indoxyl sulfate accumulation in blood and muscle. These effects contributed to decreased renal damage and delayed sarcopenia progression. Collectively, these findings suggest that lactoferrin may serve as a promising preventive and therapeutic agent for CKD-associated sarcopenia via the gut-kidney-skeletal muscle axis.
Nicotinamide ameliorates podocyte injury and albuminuria in adriamycin-induced nephropathy. International-journal Peer-reviewed

Kei Takahashi, Emiko Sato, Seiko Yamakoshi, Mizuki Ogane, Akiyo Sekimoto, Takamasa Ishikawa, Kiyomi Kisu, Yuji Oe, Koji Okamoto, Mariko Miyazaki, Tetsuhiro Tanaka, Nobuyuki Takahashi

American journal of physiology. Renal physiology　328　(4)　F501-F516　2025/04/01

DOI： 10.1152/ajprenal.00297.2024 　

More details Close

Podocytes are key components of the glomerular filtration barrier, and their injury leads to proteinuria, chronic kidney disease (CKD), and nephrotic syndrome. Effective treatments for these conditions are not well established, and prevention of podocyte injury is a crucial challenge. Nicotinamide (NAM), a form of vitamin B3, has been reported to exert beneficial effects in various renal disease models due to its antioxidant and anti-inflammatory properties and its ability to replenish nicotinamide adenine dinucleotide (NAD+). However, its impact on adriamycin (ADR)-induced nephropathy, a model of nephrotic syndrome caused by podocyte injury, remains unclear. We investigated the effects of NAM administration in a mouse model of ADR nephropathy. BALB/c mice were intravenously administered ADR to induce nephropathy. In the NAM-treated group, mice received 0.6% NAM in drinking water ad libitum starting 7 days before ADR administration. After 14 days, NAM treatment decreased albuminuria, glomerular sclerosis, and podocyte injury, and reduced inflammation and oxidative stress markers in the kidneys. NAM and NAD+ levels were decreased in ADR-treated kidneys, and the expression of the NAD+-consuming enzymes SIRT1 and PARP-1 was decreased and increased, respectively. Nicotinamide N-methyltransferase expression was increased. NAM canceled these abnormalities. In cultured rat podocytes, NAD+ alleviated ADR-induced cytotoxicity, apoptosis, and inflammation. These findings suggest that NAM prevents ADR nephropathy and podocyte injury, likely through NAD+ replenishment.
Hemodialysis employing molecular hydrogen (H2) enriched dialysis solution may improve dialysis related fatigue through impact on energy metabolism. International-journal Peer-reviewed

Masaaki Nakayama, Kimio Watanabe, Emiko Sato, Yugo Ito, Nozomi Kadota, Kasumi Konishi, Chiharu Aizawa, Yukio Maruyama, Takuya Fujimaru, Masahiko Nagahama, Fumika Taki, Michiko Suzuki

Scientific reports　15　(1)　5039-5039　2025/02/11

DOI： 10.1038/s41598-025-88827-2 　

More details Close

Hemodialysis employing molecular hydrogen (H2)-enriched dialysis solution rendered by water electrolysis (E-HD), has been reported to alleviate dialysis-related fatigue, but its association with metabolic profiles remains unclear. Eighty-one patients undergoing standard HD were classified into 3 groups [Group A (n = 25, 30.9%): fatigue with activity reduction-subgroups A1: chronic persistent fatigue (n = 11), A2: fatigue only on dialysis days (n = 14); Group B: fatigue without activity reduction (n = 24, 29.6%); Group C (n = 32, 39.5%): no fatigue], and their changes in fatigue, body composition, and metabolic profiles were studied following 12 months of E-HD. There were no significant differences in baseline characteristics among the groups. Over the 12 months after E-HD initiation, fatigue in Group A significantly decreased, while no changes in Group-B and C. Bio-impedance analysis revealed no significant changes in A1, but significant reductions in body fat and increases in skeletal muscle mass were observed despite no significant weight change in A2. Enrichment analysis suggested significant differences in metabolic pathways such as fatty acid metabolism, citric acid cycle, and glycolysis between Groups A and C at baseline, and these differences were mitigated by E-HD. E-HD could suppress dialysis-related fatigue, through possible involvement of altered energy metabolism of patients. E-HD may represent a new paradigm for uremia treatment beyond traditional solute removal-based dialysis therapies.
Conjugated fatty acids drive ferroptosis through chaperone-mediated autophagic degradation of GPX4 by targeting mitochondria. International-journal Peer-reviewed

Yusuke Hirata, Yuto Yamada, Soma Taguchi, Ryota Kojima, Haruka Masumoto, Shinnosuke Kimura, Takuya Niijima, Takashi Toyama, Ryoji Kise, Emiko Sato, Yasunori Uchida, Junya Ito, Kiyotaka Nakagawa, Tomohiko Taguchi, Asuka Inoue, Yoshiro Saito, Takuya Noguchi, Atsushi Matsuzawa

Cell death & disease　15　(12)　884-884　2024/12/06

DOI： 10.1038/s41419-024-07237-w 　

More details Close

Conjugated fatty acids (CFAs) have been known for their anti-tumor activity. However, the mechanism of action remains unclear. Here, we identify CFAs as inducers of glutathione peroxidase 4 (GPX4) degradation through chaperone-mediated autophagy (CMA). CFAs, such as (10E,12Z)-octadecadienoic acid and α-eleostearic acid (ESA), induced GPX4 degradation, generation of mitochondrial reactive oxygen species (ROS) and lipid peroxides, and ultimately ferroptosis in cancer cell lines, including HT1080 and A549 cells, which were suppressed by either pharmacological blockade of CMA or genetic deletion of LAMP2A, a crucial molecule for CMA. Mitochondrial ROS were sufficient and necessary for CMA-dependent GPX4 degradation. Oral administration of an ESA-rich oil attenuated xenograft tumor growth of wild-type, but not that of LAMP2A-deficient HT1080 cells, accompanied by increased lipid peroxidation, GPX4 degradation and cell death. Our study establishes mitochondria as the key target of CFAs to trigger lipid peroxidation and GPX4 degradation, providing insight into ferroptosis-based cancer therapy.
Generation of Thiyl Radicals in a Spatiotemporal Controlled Manner by Light: Applied for the Cis to Trans Isomerization of Unsaturated Fatty Acids/Phospholipids Peer-reviewed

Biswajit Roy, Ryota Kojima, Obaed Shah, Meg Shieh, Eshani Das, Shahrzad Ezzatpour, Emiko Sato, Yusuke Hirata, Stephen Lindahl, Atsushi Matsuzawa, Hector C. Aguilar, Ming Xian

Redox Biology　103475-103475　2024/12
Publisher: Elsevier BV
DOI： 10.1016/j.redox.2024.103475 　

ISSN： 2213-2317
Impacts of low birthweight on kidney development and intergenerational growth of the offspring Peer-reviewed

Akiyo Sekimoto, Yoko Takaso, Haruka Saruyama, Masataka Ookawa, Mari Yamamoto, Takafumi Toyohara, Daisuke Saigusa, Tomoko Fukuuchi, Mayu Otsuka, Yui Fushiki, Seiko Yamakoshi, Kayo Tanaka, Tomoaki Ikeda, Tetsuhiro Tanaka, Nobuyuki Takahashi, Eikan Mishima, Emiko Sato

iScience　111159-111159　2024/10/11
Publisher: Elsevier BV
DOI： 10.1016/j.isci.2024.111159 　

ISSN： 2589-0042
ウレミックサルコペニアにおける運動による筋細胞内代謝変化

山越聖子, 高橋知香, 森建文, 佐藤恵美子

JSBMS Letters　49　(Suppl.)　53-53　2024/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
Industrially produced <i>trans</i>-fatty acids are potent promoters of DNA damage-induced apoptosis

Yusuke Hirata, Ryota Kojima, Ryo Ashida, Yuki Nada, Shinnosuke Kimura, Emiko Sato, Takuya Noguchi, Atsushi Matsuzawa

The Journal of Toxicological Sciences　49　(1)　27-36　2024
Publisher: Japanese Society of Toxicology
DOI： 10.2131/jts.49.27 　

ISSN： 0388-1350

eISSN： 1880-3989
Changes in Metabolomic Profiles Induced by Switching from an Erythropoiesis-Stimulating Agent to a Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitor in Hemodialysis Patients: A Pilot Study Peer-reviewed

Kimio Watanabe, Emiko Sato, Eikan Mishima, Shinobu Moriya, Takuma, Skabe, Atsuya Sato, Momoko Fujiwara, Takuya Fujimaru, Yugo Ito, Fumika Taki, Masahiko Nagahama, Kenichi Tanaka, Junichiro James Kazama, Masaaki Nakayama

International Journal of Molecular Sciences　24　(16)　12752　2023/08

DOI： 10.3390/ijms241612752. 　
A comprehensive toxicological analysis of trans-fatty acids (TFAs) reveals a pro-apoptotic action specific to industrial TFAs counteracted by polyunsaturated FAs. International-journal Peer-reviewed

Yusuke Hirata, Naoki Kashiwabara, Yuki Nada, Aya Inoue, Emiko Sato, Takuya Noguchi, Atsushi Matsuzawa

Scientific reports　13　(1)　5883-5883　2023/04/11

DOI： 10.1038/s41598-023-32083-9 　

More details Close

trans-Fatty acids (TFAs) are unsaturated fatty acids containing at least one carbon-carbon double bond in trans configuration, which are classified into two groups according to their food source: industrial TFAs (iTFAs) and ruminant TFAs (rTFAs). Previous epidemiological evidence has demonstrated a preferential association of iTFAs, rather than rTFAs, with various diseases including cardiovascular diseases. However, it is still unknown how iTFAs exert their specific toxicity and what effective treatments are available to mitigate their toxicity. Here, we performed a comprehensive toxicological assessment of TFAs based on the toxicity mechanism that we established previously. We found that iTFAs including elaidic acid (EA), but not other types of fatty acids including rTFAs, had a strong pro-apoptotic effect upon treatment of extracellular ATP, a damage-associated molecular pattern that induces apoptosis through the apoptosis signal-regulating kinase 1 (ASK1)-p38 MAP kinase pathway. We also found that polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid (DHA), potently suppressed EA-dependent increase in ASK1 activation and apoptosis. These results demonstrate that iTFAs specifically exert toxicity by targeting ASK1, and that PUFAs serve as their effective suppressor. Our study provides a molecular basis for risk assessment of foods, and for new prevention and treatment strategies for TFA-related diseases.
What’s New in the Molecular Mechanisms of Diabetic Kidney Disease: Recent Advances Peer-reviewed

Kimio Watanabe, Emiko Sato, Eikan Mishima, Mariko Miyazaki, Tetsuhiro Tanaka

International Journal of Molecular Sciences　24　(1)　570-570　2022/12/29
Publisher: MDPI AG
DOI： 10.3390/ijms24010570 　

eISSN： 1422-0067

More details Close

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease, including end-stage kidney disease, and increases the risk of cardiovascular mortality. Although the treatment options for DKD, including angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, sodium-glucose cotransporter 2 inhibitors, and mineralocorticoid receptor antagonists, have advanced, their efficacy is still limited. Thus, a deeper understanding of the molecular mechanisms of DKD onset and progression is necessary for the development of new and innovative treatments for DKD. The complex pathogenesis of DKD includes various different pathways, and the mechanisms of DKD can be broadly classified into inflammatory, fibrotic, metabolic, and hemodynamic factors. Here, we summarize the recent findings in basic research, focusing on each factor and recent advances in the treatment of DKD. Collective evidence from basic and clinical research studies is helpful for understanding the definitive mechanisms of DKD and their regulatory systems. Further comprehensive exploration is warranted to advance our knowledge of the pathogenesis of DKD and establish novel treatments and preventive strategies.
A non-canonical vitamin K cycle is a potent ferroptosis suppressor. International-journal Peer-reviewed

Eikan Mishima, Junya Ito, Zijun Wu, Toshitaka Nakamura, Adam Wahida, Sebastian Doll, Wulf Tonnus, Palina Nepachalovich, Elke Eggenhofer, Maceler Aldrovandi, Bernhard Henkelmann, Ken-Ichi Yamada, Jonas Wanninger, Omkar Zilka, Emiko Sato, Regina Feederle, Daniela Hass, Adriano Maida, André Santos Dias Mourão, Andreas Linkermann, Edward K Geissler, Kiyotaka Nakagawa, Takaaki Abe, Maria Fedorova, Bettina Proneth, Derek A Pratt, Marcus Conrad

Nature　608　(7924)　778-783　2022/08

DOI： 10.1038/s41586-022-05022-3 　

More details Close

Ferroptosis, a non-apoptotic form of cell death marked by iron-dependent lipid peroxidation1, has a key role in organ injury, degenerative disease and vulnerability of therapy-resistant cancers2. Although substantial progress has been made in understanding the molecular processes relevant to ferroptosis, additional cell-extrinsic and cell-intrinsic processes that determine cell sensitivity toward ferroptosis remain unknown. Here we show that the fully reduced forms of vitamin K-a group of naphthoquinones that includes menaquinone and phylloquinone3-confer a strong anti-ferroptotic function, in addition to the conventional function linked to blood clotting by acting as a cofactor for γ-glutamyl carboxylase. Ferroptosis suppressor protein 1 (FSP1), a NAD(P)H-ubiquinone reductase and the second mainstay of ferroptosis control after glutathione peroxidase-44,5, was found to efficiently reduce vitamin K to its hydroquinone, a potent radical-trapping antioxidant and inhibitor of (phospho)lipid peroxidation. The FSP1-mediated reduction of vitamin K was also responsible for the antidotal effect of vitamin K against warfarin poisoning. It follows that FSP1 is the enzyme mediating warfarin-resistant vitamin K reduction in the canonical vitamin K cycle6. The FSP1-dependent non-canonical vitamin K cycle can act to protect cells against detrimental lipid peroxidation and ferroptosis.
尿毒素曝露下の筋細胞におけるマイオカインの影響

山越聖子, 佐藤恵美子, 高橋知香, 伊藤大樹, 遠藤明里, 矢花郁子, 阿南剛, 広瀬卓男, 木村朋由, 森建文

日本腎臓学会誌　64　(3)　221-221　2022/05
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
Methylglyoxal Induces Inflammation, Metabolic Modulation and Oxidative Stress in Myoblast Cells. International-journal Peer-reviewed

Sota Todoriki, Yui Hosoda, Tae Yamamoto, Mayu Watanabe, Akiyo Sekimoto, Hiroshi Sato, Takefumi Mori, Mariko Miyazaki, Nobuyuki Takahashi, Emiko Sato

Toxins　14　(4)　2022/04/07

DOI： 10.3390/toxins14040263 　

More details Close

Uremic sarcopenia is a serious clinical problem associated with physical disability and increased morbidity and mortality. Methylglyoxal (MG) is a highly reactive, dicarbonyl uremic toxin that accumulates in the circulatory system in patients with chronic kidney disease (CKD) and is related to the pathology of uremic sarcopenia. The pathophysiology of uremic sarcopenia is multifactorial; however, the details remain unknown. We investigated the mechanisms of MG-induced muscle atrophy using mouse myoblast C2C12 cells, focusing on intracellular metabolism and mitochondrial injury. We found that one of the causative pathological mechanisms of uremic sarcopenia is metabolic flow change to fatty acid synthesis with MG-induced ATP shortage in myoblasts. Evaluation of cell viability revealed that MG showed toxic effects only in myoblast cells, but not in myotube cells. Expression of mRNA or protein analysis revealed that MG induces muscle atrophy, inflammation, fibrosis, and oxidative stress in myoblast cells. Target metabolomics revealed that MG induces metabolic alterations, such as a reduction in tricarboxylic acid cycle metabolites. In addition, MG induces mitochondrial morphological abnormalities in myoblasts. These changes resulted in the reduction of ATP derived from the mitochondria of myoblast cells. Our results indicate that MG is a pathogenic factor in sarcopenia in CKD.
Online MS Colloquium by Kanto, Hokkaido, Tohoku and Chubu-Area Groups, and Diversity and Inclusion Committee: Lecture on Quantitative Analysis, Lab Tour, and Social Meeting

Asanuma Miwako, Kawasaki Nana, Kobayashi Yuki, Saikusa Kazumi, Sawa Ryuichi, Shimbo Kazutaka, Tanabe Kana, Nozawa Kohei, Harazono Akira, Motoyama Akira, Akutsu Hiroaki, Oka Seiko, Jin Shigeki, Takata Yusuke, Bajo Ken-ichi, Hirose Tomohiro, Mori Ayako, Saigusa Daisuke, Sato Emiko, Soga Tomoyoshi, Hirayama Akiyoshi, Maekawa Masamitsu, Mano Nariyasu, Yoshino Ken-ichi, Osaka Issey, Kurono Sadamu, Kuwata Keiko, Sakai Tatsuko, Setou Mitsutoshi, Takahashi Yutaka, Naito Yasuhide, Matsumoto Tomohiro

Journal of the Mass Spectrometry Society of Japan　70　(1)　85-89　2022/03/01
Publisher: The Mass Spectrometry Society of Japan
DOI： 10.5702/massspec.s22-18 　

ISSN： 1340-8097

eISSN： 1880-4225 1884-3271
Myeloid cell-derived coagulation tissue factor is associated with renal tubular damage in mice fed an adenine diet International-journal Peer-reviewed

Shu Yamakage, Yuji Oe, Emiko Sato, Koji Okamoto, Akiyo Sekimoto, Satoshi Kumakura, Hiroshi Sato, Mai Yoshida, Tasuku Nagasawa, Mariko Miyazaki, Sadayoshi Ito, Nigel Mackman, Nobuyuki Takahashi

Scientific Reports　11　(1)　12159-12159　2021/12
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41598-021-91586-5 　

eISSN： 2045-2322

More details Close

<title>Abstract</title>Patients with chronic kidney disease (CKD) commonly exhibit hypercoagulability. Increased levels of uremic toxins cause thrombogenicity by increasing tissue factor (TF) expression and activating the extrinsic coagulation cascade. TF is induced in monocytes and macrophages under pathological conditions, such as inflammatory diseases. However, the role of monocyte myeloid cell TF in CKD progression remains unclear. We aimed to clarify this issue, and the present study found that patients with CKD had elevated levels of D-dimer, a marker of fibrin degradation, which was associated with decreased estimated glomerular filtration rate and increased serum levels of uremic toxins, such as indoxyl sulfate. In vitro studies showed that several uremic toxins increased cellular TF levels in monocytic THP-1 cells. Mice with TF specifically deleted in myeloid cells were fed an adenine diet to cause uremic kidney injury. Myeloid TF deletion reduced tubular injury and pro-inflammatory gene expression in the kidneys of adenine-induced CKD but did not improve renal function as measured by plasma creatinine or blood urea nitrogen. Collectively, our findings suggest a novel concept of pathogenesis of coagulation-mediated kidney injury, in which elevated TF levels in monocytes under uremic conditions is partly involved in the development of CKD.
Lack of Endothelial Nitric Oxide Synthase Accelerates Ectopic Calcification in Uremic Mice Fed an Adenine and High Phosphorus Diet International-journal Peer-reviewed

Yuji Oe, Shohei Mitsui, Emiko Sato, Naoko Shibata, Kiyomi Kisu, Akiyo Sekimoto, Mariko Miyazaki, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi

The American Journal of Pathology　191　(2)　283-293　2021/02
Publisher: Elsevier BV
DOI： 10.1016/j.ajpath.2020.10.012 　

ISSN： 0002-9440

More details Close

Ectopic calcification is a risk of cardiovascular disease in chronic kidney disease (CKD) patients, and impaired endothelial nitric oxide synthase (eNOS) is involved in the CKD complications. However, whether eNOS dysfunction is a cause of ectopic calcification in CKD remains to be elucidated. To address this issue, we investigated the role of eNOS in ectopic calcification in mice with renal injury caused by an adenine and high-phosphorus (Ade + HP) diet. DBA/2J mice, a calcification-sensitive strain, were fed Ade + HP for 3 weeks. Expression levels of eNOS-related genes were reduced significantly in their calcified aorta. C57BL/6J is a calcification-resistant strain, and wild-type mice showed mild calcified lesions in the aorta and kidney when given an Ade + HP diet for 4 weeks. In contrast, a lack of eNOS led to the development of severe aortic calcification accompanied by an increase in runt-related transcription factor 2, an osteochondrogenic marker. Increased renal calcium deposition and the tubular injury score were remarkable in mice lacking eNOS-fed Ade + HP. Exacerbation of ectopic calcification by a lack of eNOS is associated with increased oxidative stress markers such as nicotinamide adenine dinucleotide phosphate oxidases. In conclusion, eNOS is critically important in preventing ectopic calcification. Therefore, the maintenance of eNOS is useful to reduce cardiovascular disease events and to improve prognosis in CKD patients.
Effect of uremic toxins on hippocampal cell damage: analysis in vitro and in rat model of chronic kidney disease International-journal

Kimio Watanabe, Emiko Sato, Eikan Mishima, Mayu Watanabe, Takaaki Abe, Nobuyuki Takahashi, Masaaki Nakayama

Heliyon　7　(2)　e06221-e06221　2021/02
Publisher: Elsevier BV
DOI： 10.1016/j.heliyon.2021.e06221 　

ISSN： 2405-8440

More details Close

One third of the patients with chronic kidney disease (CKD) develop cognitive impairment, which is also an independent risk factor for mortality. However, the concise mechanism of cerebro-renal interaction has not been clarified. The present study examines the effects of uremic toxins on neuronal cells and analyzes the pathological condition of the brain using mouse hippocampal neuronal HT-22 cells and adenine-induced CKD model rats. Among the uremic toxins analyzed, indoxyl sulfate, indole, 3-indoleacetate, and methylglyoxal significantly decreased viability and glutathione level in HT-22 cells. The mixture of these uremic toxins also decreased viability and glutathione level at a lower dose. Adenine-induced CKD rat showed marked renal damage, increased urinary oxidative stress markers, and increased numbers of pyknotic neuronal cells in hippocampus. CKD rats with damaged hippocampus demonstrated poor learning process when tested using the Morris water maze test. Our results suggest that uremic toxins have a toxic effect on hippocampal neuronal cells and uremic CKD rats shows pyknosis in hippocampus.
Nicotinamide Attenuates the Progression of Renal Failure in a Mouse Model of Adenine-Induced Chronic Kidney Disease International-journal Invited Peer-reviewed

Satoshi Kumakura, Emiko Sato, Akiyo Sekimoto, Yamato Hashizume, Shu Yamakage, Mariko Miyazaki, Sadayoshi Ito, Hideo Harigae, Nobuyuki Takahashi

Toxins　13　(1)　50-50　2021/01/11
Publisher: MDPI AG
DOI： 10.3390/toxins13010050 　

eISSN： 2072-6651

More details Close

Nicotinamide adenine dinucleotide (NAD+) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation. In this study, the role of NAD+ in kidney disease was investigated through the supplementation of nicotinamide (Nam), a precursor of NAD+, to an adenine-induced CKD mouse model. Nam supplementation reduced kidney inflammation and fibrosis and, therefore, prevented the progression of kidney disease. Notably, Nam supplementation also attenuated the accumulation of glycolysis and Krebs cycle metabolites that occurs in renal failure. These effects were due to increased NAD+ supply, which accelerated NAD+-consuming metabolic pathways. Our study suggests that Nam administration may be a novel therapeutic approach for CKD prevention.
The effect of aldosterone on adiposity - The role of glucose absorption in the small intestine International-journal Peer-reviewed

Hidekazu Shirai, Emiko Sato, Akiyo Sekimoto, Taeko Uchida, Yuji Oe, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

Biochemical and Biophysical Research Communications　531　(4)　628-635　2020/10
Publisher: Elsevier BV
DOI： 10.1016/j.bbrc.2020.07.119 　

ISSN： 0006-291X

More details Close

We have previously demonstrated that manipulation of the renin angiotensin system (RAS) has large effects on digestive efficiency. However, the effects of aldosterone on body weight, adiposity, and glucose absorption in the intestine remains unknown. We here demonstrated that lack of aldosterone synthase (ASKO) in mice did not affect adiposity. In contrast, mice administered with aldosterone were resistant to diet-induced obesity. This is due to gastrointestinal loss of dietary glucose. As expected, ASKO mice had increased glucose absorption, whereas mice administered with aldosterone had reduced glucose absorption in the small intestine. Furthermore, the level of protein expression of sodium glucose transporter 1 (SGLT1) in the mucosa of the jejunum was higher in ASKO mice, and lower in mice administered with aldosterone than control mice. Our findings indicate that aldosterone plays an important role on SGLT-1-mediated glucose absorption in the small intestine.
Metabolomics of a mouse model of preeclampsia induced by overexpressing soluble fms-like tyrosine kinase 1. International-journal Peer-reviewed

Emiko Sato, Yukako Tsunokuni, Manami Kaneko, Daisuke Saigusa, Ritsumi Saito, Shuichi Shimma, Akiyo Sekimoto, Yoshiko Kawana, Yuji Oe, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

Biochemical and biophysical research communications　527　(4)　1064-1071　2020/07/05

DOI： 10.1016/j.bbrc.2020.04.079 　

More details Close

Preeclampsia (PE) is a leading cause of maternal morbidity and mortality. Nicotinamide has beneficial effects on PE. In this study, we evaluated the effect of nicotinamide on placental development using a PE mouse model. To generate the PE model, a recombinant adenovirus to overproduce soluble fms-like tyrosine kinase 1 (sFlt-1) was administered to mice (Jcl:ICR) at 8.5 day post-coitum (dpc). Plasma and placenta samples were harvested at 12.5 dpc. Fetal and placental weight was significantly decreased at 12.5 dpc in PE mice. Plasma and placental acylcarnitine levels were significantly higher in PE mice than those in control mice. Glycolysis was accelerated and glucose metabolic flow was altered with hypoxia, leading to ATP shortage in the labyrinth of PE mice. In PE mice, ATP production was diminished, and fatty acid oxidation was accelerated in the placenta, consequently, blood carnitine and acylcarnitine levels were increased. The mitochondrial morphology in BeWo cells was impaired under hypoxia. Nicotinamide treatment reversed fetal growth restriction, placental development, and altered metabolic flow in the early stage in PE. In addition, nicotinamide normalized impaired mitochondrial morphology. Hence, targeting this metabolic alteration in the placenta using nicotinamide may serve as a potential therapeutic approach for PE treatment.
Protease-activated receptor 2 contributes to placental development and fetal growth in mice. International-journal Peer-reviewed

Shu Yamakage, Yuji Oe, Akiyo Sekimoto, Hirofumi Obata, Miho Yasuta, Emiko Sato, Satoshi Kumakura, Hiroshi Sato, Junichi Sugawara, Sadayoshi Ito, Nobuyuki Takahashi

Thrombosis research　193　173-179　2020/07/02

DOI： 10.1016/j.thromres.2020.06.039 　

More details Close

BACKGROUND: Protease-activated receptor 2 (PAR2) is activated by serine proteases such as coagulation tissue factor/VIIa complex, factor Xa or trypsin and is pro-angiogenic in several disease models. Impaired angiogenesis in placenta causes placental dysfunction and fetal growth restriction. PAR2 is expressed in the placenta trophoblast. However, the role of PAR2 in pregnancy remains unknown. OBJECTIVE: The present study aimed to examine the role of PAR2 in placental development and fetal growth using a murine model. METHODS: PAR2-/- or PAR2+/+ mice in the ICR background were used. Female PAR2-/- mice were mated with male PAR2-/- mice, and female PAR2+/+ mice were mated with male PAR2+/+ mice to obtain PAR2-/- and PAR2+/+ fetuses, respectively. The day a virginal plug was observed in the morning was determined as 0.5-day post-coitum (dpc). Pregnant mice were sacrificed on 13.5 or 18.5 dpc to collect samples. RESULTS: A deficiency of PAR2 significantly reduced the fetal and placental weight and impaired placental labyrinth development in mice on 18.5 dpc. Collagen IV expression in placenta labyrinth was smaller in PAR2 knockout mice compared to that of wild-type mice. A deficiency of PAR2 also reduced the expression levels of genes related to angiogenesis and coagulation in placenta. CONCLUSION: Our data suggest that PAR2 is required for fetal growth and angiogenesis in the placenta and is thus important for a normal pregnancy.
Dual Blockade of Protease-Activated Receptor 1 and 2 Additively Ameliorates Diabetic Kidney Disease Peer-reviewed

Shohei Mitsui, Yuji Oe, Akiyo Sekimoto, Emiko Sato, Yamato Hashizume, Shu Yamakage, Satoshi Kumakura, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi

American Journal of Physiology Renal Physiology　318　(5)　F1067-F1073　2020/04
Uremic toxins alter coagulation and fibrinolysis-related genes expression in human endothelial cells

Yuji Oe, Emiko Sato, Hiroshi Sato, Mariko Miyazaki, Sadayoshi Ito, Nobuyuki Takahashi

Thrombosis Research　186　75-77　2020/02
Publisher: Elsevier BV
DOI： 10.1016/j.thromres.2019.12.017 　

ISSN： 0049-3848
Drugs Repurposed as Antiferroptosis Agents Suppress Organ Damage, Including AKI, by Functioning as Lipid Peroxyl Radical Scavengers. International-journal Peer-reviewed

Eikan Mishima, Emiko Sato, Junya Ito, Ken-Ichi Yamada, Chitose Suzuki, Yoshitsugu Oikawa, Tetsuro Matsuhashi, Koichi Kikuchi, Takafumi Toyohara, Takehiro Suzuki, Sadayoshi Ito, Kiyotaka Nakagawa, Takaaki Abe

Journal of the American Society of Nephrology : JASN　31　(2)　280-296　2020/02

DOI： 10.1681/ASN.2019060570 　

More details Close

BACKGROUND: Ferroptosis, nonapoptotic cell death mediated by free radical reactions and driven by the oxidative degradation of lipids, is a therapeutic target because of its role in organ damage, including AKI. Ferroptosis-causing radicals that are targeted by ferroptosis suppressors have not been unequivocally identified. Because certain cytochrome P450 substrate drugs can prevent lipid peroxidation via obscure mechanisms, we evaluated their antiferroptotic potential and used them to identify ferroptosis-causing radicals. METHODS: Using a cell-based assay, we screened cytochrome P450 substrate compounds to identify drugs with antiferroptotic activity and investigated the underlying mechanism. To evaluate radical-scavenging activity, we used electron paramagnetic resonance-spin trapping methods and a fluorescence probe for lipid radicals, NBD-Pen, that we had developed. We then assessed the therapeutic potency of these drugs in mouse models of cisplatin-induced AKI and LPS/galactosamine-induced liver injury. RESULTS: We identified various US Food and Drug Administration-approved drugs and hormones that have antiferroptotic properties, including rifampicin, promethazine, omeprazole, indole-3-carbinol, carvedilol, propranolol, estradiol, and thyroid hormones. The antiferroptotic drug effects were closely associated with the scavenging of lipid peroxyl radicals but not significantly related to interactions with other radicals. The elevated lipid peroxyl radical levels were associated with ferroptosis onset, and known ferroptosis suppressors, such as ferrostatin-1, also functioned as lipid peroxyl radical scavengers. The drugs exerted antiferroptotic activities in various cell types, including tubules, podocytes, and renal fibroblasts. Moreover, in mice, the drugs ameliorated AKI and liver injury, with suppression of tissue lipid peroxidation and decreased cell death. CONCLUSIONS: Although elevated lipid peroxyl radical levels can trigger ferroptosis onset, some drugs that scavenge lipid peroxyl radicals can help control ferroptosis-related disorders, including AKI.
Tadalafil alleviates preeclampsia and fetal growth restriction in RUPP model of preeclampsia in mice. International-journal Peer-reviewed

Akiyo Sekimoto, Kayo Tanaka, Yamato Hashizume, Emiko Sato, Hiroshi Sato, Tomoaki Ikeda, Nobuyuki Takahashi

Biochemical and biophysical research communications　521　(3)　769-774　2020/01/15

DOI： 10.1016/j.bbrc.2019.10.186 　

More details Close

BACKGROUND: - Tadalafil, a long-acting phosphodiesterase 5 (PDE5) inhibitor, alleviates preeclampsia (PE), and decreases the fetal and infant deaths associated with fetal growth restriction (FGR) in phase II clinical trial. Recently, we demonstrated that tadalafil alleviates FGR and hypertension in the dams with PE induced by l-NAME. OBJECTIVE: -The aim of present study was to clarify the effect of tadalafil in another mouse model of PE, murine reduced uterine perfusion pressure (RUPP) model we have recently developed. METHODS: -At 14.5 dpc we performed RUPP operation in mice to induce PE, administered the animals with tadalafil or vehicle in the drinking water daily from 15.5 dpc, and sacrificed them at 18.5 dpc for analyses. RESULTS: -Tadalafil improved maternal hypertension and glomerular endotheliosis in RUPP mice. Moreover, tadalafil prolonged pregnancy period, and improved survival and growth of the embryos. RUPP increased content of sFlt-1 protein in the placenta, and tadalafil corrected it back to control levels. CONCLUSION: - Tadalafil alleviates PE-like phenotype and FGR in RUPP murine model. RUPP model could help understand the mechanism of how tadalafil works on PE and FGR.
導入期腎不全患者における糖化反応中間体の影響

山本多恵, 佐藤恵美子, 大和留美子, 藤倉恵美, 吉田舞, 佐藤博, 伊藤貞嘉, 宮崎真理子

日本腎臓学会誌　61　(3)　307-307　2019/05
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
Hydrochlorothiazide ameliorates polyuria caused by tolvaptan treatment of polycystic kidney disease in PCK rats. Peer-reviewed

Anyi Wang, Takuo Hirose, Yusuke Ohsaki, Chika Takahashi, Emiko Sato, Ikuko Oba-Yabana, Satoshi Kinugasa, Yoshikazu Muroya, Sadayoshi Ito, Takefumi Mori

Clinical and experimental nephrology　23　(4)　455-464　2019/04

DOI： 10.1007/s10157-018-1669-9 　

ISSN： 1342-1751

More details Close

BACKGROUND: Tolvaptan is an effective treatment for polycystic kidney disease (PKD), but also causes unfortunate polyuria. Hydrochlorothiazide (HCTZ) has been shown to reduce urine volume in nephrogenic diabetes insipidus, raising the possibility that HCTZ could also be effective in reducing tolvaptan-induced polyuria. In this study, we examined the combined administration of HCTZ and tolvaptan. METHODS: Male PCK rats were divided into four groups of normal chow (Cont), normal chow plus tolvaptan, gavage HCTZ treatment, and tolvaptan + HCTZ. Biochemical examinations of the plasma and urine were performed as well as histological and molecular (mRNA and protein expression) analyses. RESULTS: Groups treated with tolvaptan had significantly higher 24 h urine excretion, which was significantly reduced in the tolvaptan + HCTZ group after 2 weeks. Cyst size, pERK protein expression, and Cyclin D1 mRNA expression were all significantly reduced in both the tolvaptan and tolvaptan + HCTZ groups, indicating that HCTZ did not affect the beneficial functions of tolvaptan. Notably, aquaporin 2 redistribution from the apical to intracellular domains was observed in tolvaptan-treated rats and was partially reversed in the tolvaptan + HCTZ group. The renal glomerular filtration rate was reduced in the tolvaptan + HCTZ group. Significantly lowered mRNA expression of neuronal nitric oxide synthase, prostaglandin E synthase 2 and renin were also found in the medulla, but not in the cortex. CONCLUSION: HCTZ reduces tolvaptan-induced polyuria without altering its beneficial effects on PKD. This novel therapeutic combination could potentially lead to better PKD treatments and improved quality of life for the affected patients.
Nicotinamide alleviates kidney injury and pregnancy outcomes in lupus-prone MRL/lpr mice treated with lipopolysaccharide. Peer-reviewed

Imaruoka K, Oe Y, Fushima T, Sato E, Sekimoto A, Sato H, Sugawara J, Ito S, Takahashi N

Biochemical and biophysical research communications　510　(4)　587-593　2019/02
Publisher: Elsevier BV
DOI： 10.1016/j.bbrc.2019.01.110 　

ISSN： 0006-291X
Glomerular Injury Is Exacerbated in Lupus-Prone MRL/lpr Mice Treated with a Protease-Activated Receptor 2 Antagonist

Rina Itto, Yuji Oe, Kenta Imaruoka, Emiko Sato, Akiyo Sekimoto, Shu Yamakage, Satoshi Kumakura, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi

The Tohoku Journal of Experimental Medicine　249　(2)　127-133　2019
Publisher: Tohoku University Medical Press
DOI： 10.1620/tjem.249.127 　

ISSN： 0040-8727

eISSN： 1349-3329

More details Close

Systemic lupus erythematosus (SLE) is characterized by the production of autoantibodies, which causes multi-organ injury such as lupus nephritis. SLE is associated with hypercoagulability. Activated coagulation factors such as tissue factor and VIIa complex and factor Xa activate protease-activated receptor 2 (PAR2). PAR2 promotes cytokine production through mitogen-activated protein kinase or nuclear factor kappa B signaling, and previous reports demonstrated that inhibition of PAR2 alleviated kidney injuries such as diabetic kidney disease and renal fibrosis in animal models. However, the involvement of PAR2 in the pathogenesis of SLE remains unclear. We therefore administered a selective PAR2 peptide antagonist, FSLLRY-NH2, to SLE-prone 4-month-old MRL-Faslpr mice for 4 weeks. Treatment with FSLLRY-NH2 caused the significant increases in the glomerular mesangial proliferation, glomerular deposition of both immunoglobulin G and complement factor C3d, and glomerular infiltration of Mac2-positive macrophages and CD3-positive T cells, compared with MRL-Faslpr mice treated with saline. In addition, the treatment with the PAR2 antagonist increased renal expression levels of tumor necrosis factor-α (Tnfa) and monocyte chemoattractant protein 1 (Mcp1) mRNA. Collectively, these results suggest that inhibition of PAR2 may increase the severity of inflammation in lupus nephritis; namely, opposite to previous observations, PAR2 has anti-inflammatory properties. We propose that activation of PAR2 could serve as a potential therapeutic option for patients with SLE.
Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury. Peer-reviewed

Oe Y, Fushima T, Sato E, Sekimoto A, Kisu K, Sato H, Sugawara J, Ito S, Takahashi N

Sci Rep　9　(1)　2986　2019
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41598-019-39914-8 　

eISSN： 2045-2322
Protease-activated receptor 2 exacerbates cisplatin-induced nephrotoxicity. Peer-reviewed

Watanabe M, Oe Y, Sato E, Sekimoto A, Sato H, Ito S, Takahashi N

American journal of physiology. Renal physiology　316　(4)　F654-F659　2019/01
Publisher: American Physiological Society
DOI： 10.1152/ajprenal.00489.2018 　

ISSN： 1931-857X

eISSN： 1522-1466

More details Close

Acute kidney injury (AKI) is associated with hypercoagulability. Tissue factor/factor VIIa complex and factor Xa in the coagulation cascade activate protease-activated receptor 2 (PAR2). Previously, we have shown that PAR2-mediated inflammation aggravates kidney injury in models of diabetic kidney disease and adenine-induced renal fibrosis. However, the role of PAR2 in AKI remains unclear. To clarify the role of PAR2, we administered cisplatin, one of the most common causal factors of AKI, to wild-type and PAR2-deficient mice. The expression levels of tissue factor and PAR2 were significantly increased in the kidneys of mice that were administered cisplatin. A lack of PAR2 corrected the levels of plasma blood urea nitrogen and creatinine as well as ameliorated the acute tubular injury score in the kidney. A lack of PAR2 corrected the infiltration of neutrophils and the gene expression levels of proinflammatory cytokines/chemokines in these mouse kidneys. Similarly, apoptotic markers, such as cleaved caspase-3-positive area and Bax/Bcl2 ratio, were attenuated via PAR2 deletion. Thus, elevated PAR2 exacerbates cisplatin nephrotoxicity, and targeting PAR2 is a novel therapeutic option that aids in the treatment of patients with cisplatin-induced AKI.
Hepatic dysfunction and thrombocytopenia induced by excess sFlt1 in mice lacking endothelial nitric oxide synthase Peer-reviewed

Yuji Oe, Mieko Ko, Tomofumi Fushima, Emiko Sato, S. Ananth Karumanchi, Hiroshi Sato, Junichi Sugawara, Sadayoshi Ito, Nobuyuki Takahashi

Scientific Reports　8　(1)　2018/12/01

DOI： 10.1038/s41598-017-18260-7 　

ISSN： 2045-2322
(Pro)renin receptor is involved in mesangial fibrosis and matrix expansion Peer-reviewed

Kaori Narumi, Emiko Sato, Takuo Hirose, Tae Yamamoto, Takashi Nakamichi, Mariko Miyazaki, Hiroshi Sato, Sadayoshi Ito

Scientific Reports　8　(1)　2018/12/01

DOI： 10.1038/s41598-017-18314-w 　

ISSN： 2045-2322
Acidic organelles mediate TGF-β1-induced cellular fibrosis via (pro)renin receptor and vacuolar ATPase trafficking in human peritoneal mesothelial cells Peer-reviewed

Ikuko Oba-Yabana, Takefumi Mori, Chika Takahashi, Takuo Hirose, Yusuke Ohsaki, Satoshi Kinugasa, Yoshikazu Muroya, Emiko Sato, Geneviève Nguyen, Rémi Piedagnel, Pierre M. Ronco, Kazuhito Totsune, Sadayoshi Ito

Scientific Reports　8　(1)　2018/12/01

DOI： 10.1038/s41598-018-20940-x 　

ISSN： 2045-2322
Pathophysiological and molecular mechanisms involved in renal congestion in a novel rat model. International-journal Peer-reviewed

Satoshi Shimada, Takuo Hirose, Chika Takahashi, Emiko Sato, Satoshi Kinugasa, Yusuke Ohsaki, Kiyomi Kisu, Hiroshi Sato, Sadayoshi Ito, Takefumi Mori

Scientific reports　8　(1)　16808-16808　2018/11/14

DOI： 10.1038/s41598-018-35162-4 　

More details Close

Increased central venous pressure in congestive heart failure causes renal dysfunction; however, the underlying mechanisms are unclear. We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
ニコチンアミドは妊娠SLEマウスにおける腎・妊娠予後を改善させる

大江佑治, 伊丸岡健太, 伏間智史, 堰本晃代, 佐藤恵美子, 菅原準一, 佐藤博, 伊藤貞嘉, 高橋信行

日本妊娠高血圧学会雑誌　25　73-73　2018/11
Publisher: (一社)日本妊娠高血圧学会
ISSN： 1880-3172
ニコチンアミドは妊娠SLEマウスにおける腎・妊娠予後を改善させる

大江佑治, 伊丸岡健太, 伏間智史, 堰本晃代, 佐藤恵美子, 菅原準一, 佐藤博, 伊藤貞嘉, 高橋信行

日本高血圧学会総会プログラム・抄録集　41回　SHRY-03　2018/09
Publisher: (NPO)日本高血圧学会
Urinary Angiotensinogen Excretion Level Is Associated With Elevated Blood Pressure in the Normotensive General Population International-journal Peer-reviewed

Sato Emiko, Wang An Yi, Satoh Michihiro, Nishikiori Yoko, Oba-Yabana Ikuko, Yoshida Mai, Sato Hiroshi, Ito Sadayoshi, Hida Wataru, Mori Takefumi

AMERICAN JOURNAL OF HYPERTENSION　31　(6)　742-749　2018/06

DOI： 10.1093/ajh/hpy020 　

ISSN： 0895-7061
Vitamin B3 nicotinamide: A promising candidate for treating preeclampsia and improving fetal growth Peer-reviewed

Nobuyuki Takahashi, Feng Li, Tomofumi Fushima, Gen Oyanagi, Emiko Sato, Yuji Oe, Akiyo Sekimoto, Daisuke Saigusa, Hiroshi Sato, Sadayoshi Ito

Tohoku Journal of Experimental Medicine　244　(3)　243-248　2018/03/01

DOI： 10.1620/tjem.244.243 　

ISSN： 1349-3329 0040-8727
Impact of the Oral Adsorbent AST-120 on Organ-Specific Accumulation of Uremic Toxins: LC-MS/MS and MS Imaging Techniques. International-journal Peer-reviewed

Emiko Sato, Daisuke Saigusa, Eikan Mishima, Taeko Uchida, Daisuke Miura, Tomomi Morikawa-Ichinose, Kiyomi Kisu, Akiyo Sekimoto, Ritsumi Saito, Yuji Oe, Yotaro Matsumoto, Yoshihisa Tomioka, Takefumi Mori, Nobuyuki Takahashi, Hiroshi Sato, Takaaki Abe, Toshimitsu Niwa, Sadayoshi Ito

Toxins　10　(1)　2017/12/28

DOI： 10.3390/toxins10010019 　

ISSN： 2072-6651
Nicotinamide ameliorates a preeclampsia-like condition in mice with reduced uterine perfusion pressure Peer-reviewed

Tomofumi Fushima, Akiyo Sekimoto, Yuji Oe, Emiko Sato, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY　312　(2)　F366-F372　2017/02

DOI： 10.1152/ajprenal.00501.2016 　

ISSN： 1931-857X

eISSN： 1522-1466
Nicotinamide ameliorates a preeclampsia-like condition in mice with reduced uterine perfusion pressure Peer-reviewed

Tomofumi Fushima, Akiyo Sekimoto, Yuji Oe, Emiko Sato, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

American Journal of Physiology - Renal Physiology　312　(2)　F366-F372　2017
Publisher: American Physiological Society
DOI： 10.1152/ajprenal.00501.2016 　

ISSN： 1522-1466 0363-6127
Protease-activated receptor 2 exacerbates adenine-induced renal tubulointerstitial injury in mice Peer-reviewed

Sakiko Hayashi, Yuji Oe, Tomofumi Fushima, Emiko Sato, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　483　(1)　547-552　2017/01

DOI： 10.1016/j.bbrc.2016.12.108 　

ISSN： 0006-291X

eISSN： 1090-2104
Metabolic alterations by indoxyl sulfate in skeletal muscle induce uremic sarcopenia in chronic kidney disease Peer-reviewed

Emiko Sato, Takefumi Mori, Eikan Mishima, Arisa Suzuki, Sanae Sugawara, Naho Kurasawa, Daisuke Saigusa, Daisuke Miura, Tomomi Morikawa-Ichinose, Ritsumi Saito, Ikuko Oba-Yabana, Yuji Oe, Kiyomi Kisu, Eri Naganuma, Kenji Koizumi, Takayuki Mokudai, Yoshimi Niwano, Tai Kudo, Chitose Suzuki, Nobuyuki Takahashi, Hiroshi Sato, Takaaki Abe, Toshimitsu Niwa, Sadayoshi Ito

SCIENTIFIC REPORTS　6　2016/11

DOI： 10.1038/srep36618 　

ISSN： 2045-2322
Nicotinamide benefits both mothers and pups in two contrasting mouse models of preeclampsia Peer-reviewed

Feng Li, Tomofumi Fushima, Gen Oyanagi, H. W. Davin Townley-Tilson, Emiko Sato, Hironobu Nakada, Yuji Oe, John R. Hagaman, Jennifer Wilder, Manyu Li, Akiyo Sekimoto, Daisuke Saigusa, Hiroshi Sato, Sadayoshi Ito, J. Charles Jennette, Nobuyo Maeda, S. Ananth Karumanchi, Oliver Smithies, Nobuyuki Takahashi

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　113　(47)　13450-13455　2016/11

DOI： 10.1073/pnas.1614947113 　

ISSN： 0027-8424
Comparisons of amino acids, body constituents and antioxidative response between long-time HD and normal HD Peer-reviewed

Akira Torigoe, Emiko Sato, Takefumi Mori, Norio Ieiri, Chika Takahashi, Yoko Ishida, Osamu Hotta, Sadayoshi Ito

HEMODIALYSIS INTERNATIONAL　20　S17-S24　2016/10

DOI： 10.1111/hdi.12462 　

ISSN： 1492-7535

eISSN： 1542-4758
PIVOTAL ROLE OF HEME OXYGENASE IN AMELIORATION BY NICOTINAMIDE OF FETAL GROWTH RESTRICTION ASSOCIATED WITH PREECLAMPSIA Peer-reviewed

Nakada Hironobu, Fushima Tomofumi, Sekimoto Akiyo, Oe Yuji, Sato Emiko, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E236　2016/09

DOI： 10.1097/01.hjh.0000500524.43340.2b 　

ISSN： 0263-6352
NOVEL REDUCED UTERINE PERFUSION PRESSURE (RUPP) MODEL OF PREECLAMPSIA IN MICE Peer-reviewed

Fushima Tomofumi, Sekimoto Akiyo, Minato Takahiro, Ito Takuya, Oe Yuji, Kisu Kiyomi, Sato Emiko, Funamoto Kenichi, Kimura Yoshitaka, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E237　2016/09

DOI： 10.1097/01.hjh.0000500527.66210.66 　

ISSN： 0263-6352
METABOLOMIC ANALYSIS OF A MOUSE MODEL OF PREECLAMPSIA INDUCED BY OVERPRODUCING sFLt-1 Peer-reviewed

Sato Emiko, Tsunokuni Yukako, Fushima Tomofumi, Kaneko Manami, Saito Ritsumi, Sekimoto Akiyo, Saigusa Daisuke, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E69　2016/09

DOI： 10.1097/01.hjh.0000500031.24401.46 　

ISSN： 0263-6352
APPLICATION OF NOVEL REDUCED UTERINE PERFUSION PRESSURE (RUPP) MODEL OF PREECLAMPSIA IN C57BL/6J MICE Peer-reviewed

Sekimoto Akiyo, Fushima Tomofumi, Oe Yuji, Kisu Kiyomi, Sato Emiko, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E409　2016/09

DOI： 10.1097/01.hjh.0000501052.07978.d5 　

ISSN： 0263-6352
IGA NEPHROPATHY IS EXACERBATED BY PREGNANCY AND IS A RISK FACTOR FOR PREECLAMPSIA IN GROUPED DDY MICE Peer-reviewed

Fushima Tomofumi, Oe Yuji, Sato Emiko, Suzuki Yusuke, Tomino Yasuhiko, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E427　2016/09

DOI： 10.1097/01.hjh.0000501101.72126.01 　

ISSN： 0263-6352
PAR2 SIGNALING EXACERBATES DIABETIC NEPHROPATHY Peer-reviewed

Oe Yuji, Hayashi Sakiko, Fushima Tomofumi, Sato Emiko, Kisu Kiyomi, Sato Hiroshi, Ito Sadayoshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E326　2016/09

DOI： 10.1097/01.hjh.0000500812.17722.74 　

ISSN： 0263-6352
INHIBITING PROTEASE-ACTIVATED RECEPTOR 2 ALLEVIATED PREECLAMPSIA Peer-reviewed

Takahashi Nobuyuki, Ko Mieko, Oe Yuji, Fushima Tomofumi, Sekimoto Akiyo, Sato Emiko, Ito Sadayoshi, Sato Hiroshi

JOURNAL OF HYPERTENSION　34　E101　2016/09

DOI： 10.1097/01.hjh.0000500120.73302.2e 　

ISSN： 0263-6352
AN ORAL FACTOR XA INHIBITOR, EDOXABAN, ALLEVIATES DIABETIC NEPHROPATHY IN MICE LACKING eNOS Peer-reviewed

Oe Yuji, Fushima Tomofumi, Sato Emiko, Sato Hiroshi, Ito Sadayoshi, Takahashi Nobuyuki

JOURNAL OF HYPERTENSION　34　E102　2016/09

DOI： 10.1097/01.hjh.0000500125.77396.fa 　

ISSN： 0263-6352
A simple and rapid ultra-high-performance liquid chromatography-tandem mass spectrometry method to determine plasma biotin in hemodialysis patients Peer-reviewed

Shigeaki Yagi, Manabu Nishizawa, Itiro Ando, Shiro Oguma, Emiko Sato, Yutaka Imai, Masako Fujiwara

BIOMEDICAL CHROMATOGRAPHY　30　(8)　1285-1290　2016/08

DOI： 10.1002/bmc.3680 　

ISSN： 0269-3879

eISSN： 1099-0801
Coagulation Factor Xa and Protease-Activated Receptor 2 as Novel Therapeutic Targets for Diabetic Nephropathy Peer-reviewed

Yuji Oe, Sakiko Hayashi, Tomofumi Fushima, Emiko Sato, Kiyomi Kisu, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY　36　(8)　1525-1533　2016/08

DOI： 10.1161/ATVBAHA.116.307883 　

ISSN： 1079-5642

eISSN： 1524-4636
Reduced Uterine Perfusion Pressure (RUPP) Model of Preeclampsia in Mice Peer-reviewed

Tomofumi Fushima, Akiyo Sekimoto, Takahiro Minato, Takuya Ito, Yuji Oe, Kiyomi Kisu, Emiko Sato, Kenichi Funamoto, Toshiyuki Hayase, Yoshitaka Kimura, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

PLOS ONE　11　(5)　2016/05

DOI： 10.1371/journal.pone.0155426 　

ISSN： 1932-6203
脂肪細胞由来の未知のアルドステロン合成酵素(CYP11B2)発現誘導因子の探索

島田洋樹, 伊藤亮, 佐藤恵美子, 横山敦, 菅原明

日本内分泌学会雑誌　92　(1)　216-216　2016/04
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
Circulation Peer-reviewed

Daisuke Ito, Pengyu Cao, Takaaki Kakihana, Emiko Sato, Yoshikazu Muroya, Yoshiko Ogawa, Gaizun Hu, Tadashi Ishii, Osamu Ito, Masahiro Kohzuki, Hideyasu Kiyomoto

CIRCULATION　133　2016/03

ISSN： 0009-7322

eISSN： 1524-4539
Urinary angiotensinogen excretion is associated with blood pressure in obese young adults Peer-reviewed

Emiko Sato, Takefumi Mori, Michihiro Satoh, Mutsuko Fujiwara, Yoshimi Nakamichi, Ikuko Oba, Susumu Ogawa, Yoshitaka Kinouchi, Hiroshi Sato, Sadayoshi Ito, Wataru Hida

CLINICAL AND EXPERIMENTAL HYPERTENSION　38　(2)　203-208　2016/02

DOI： 10.3109/10641963.2015.1081219 　

ISSN： 1064-1963

eISSN： 1525-6006
Efficacy and Biocompatibility of Neutral Icodextrin Peritoneal Dialysis Fluid. Peer-reviewed

Shimada S, Mori T, Koizumi K, Sato S, Oba-Yabana I, Ohsaki Y, Sato E, Naganuma E, Kurasawa N, Tsuchikawa M, Ito S

Adv Perit Dial　32　46-50　2016
Role of Chronic Use of Tolvaptan in Patients with Heart Failure Undergoing Peritoneal Dialysis. Peer-reviewed

Mori T, Kurasawa N, Ohsaki Y, Koizumi K, Sato S, Oba-Yabana I, Shimada S, Sato E, Naganuma E, Tsuchikawa M, Ito S

Adv Perit Dial　32　39-45　2016
A novel and sensitive assay for heme oxygenase activity Peer-reviewed

Saki Iwamori, Emiko Sato, Daisuke Saigusa, Kouichi Yoshinari, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY　309　(7)　F667-F671　2015/10

DOI： 10.1152/ajprenal.00210.2015 　

ISSN： 1931-857X

eISSN： 1522-1466
Novel method for immunofluorescence staining of mammalian eggs using non-contact alternating-current electric-field mixing of microdroplets Peer-reviewed

Shirasawa Hiromitsu, Kumagai Jin, Sato Emiko, Kabashima Katsuya, Kumazawa Yukiyo, Sato Wataru, Miura Hiroshi, Nakamura Ryuta, Nanjo Hiroshi, Minamiya Yoshihiro, Akagami Yoichi, Terada Yukihiro

SCIENTIFIC REPORTS　5　2015/10

DOI： 10.1038/srep15371 　

ISSN： 2045-2322
Zucker diabetic fattyラットにおける長期的運動の腎酸化ストレス系への影響

伊藤大亮, 曹鵬宇, 柿花隆昭, 佐藤恵美子, 胡丐尊, 室谷嘉一, 小川佳子, 伊藤修, 上月正博, 清元秀泰

日本内分泌学会雑誌　91　(2)　646-646　2015/09
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
A novel and sensitive assay for heme oxygenase activity Peer-reviewed

Saki Iwamori, Emiko Sato, Daisuke Saigusa, Kouichi Yoshinari, Sadayoshi Ito, Hiroshi Sato, Nobuyuki Takahashi

American Journal of Physiology - Renal Physiology　309　(7)　F667-F671　2015/09/01
Publisher: American Physiological Society
DOI： 10.1152/ajprenal.00210.2015 　

ISSN： 1522-1466 0363-6127
Chronic Running Exercise Alleviates Early Progression of Nephropathy with Upregulation of Nitric Oxide Synthases and Suppression of Glycation in Zucker Diabetic Rats Peer-reviewed

Daisuke Ito, Pengyu Cao, Takaaki Kakihana, Emiko Sato, Chihiro Suda, Yoshikazu Muroya, Yoshiko Ogawa, Gaizun Hu, Tadashi Ishii, Osamu Ito, Masahiro Kohzuki, Hideyasu Kiyomoto

PLOS ONE　10　(9)　2015/09

DOI： 10.1371/journal.pone.0138037 　

ISSN： 1932-6203
A functional (pro)renin receptor is expressed in human lymphocytes and monocytes Peer-reviewed

Kaori Narumi, Takuo Hirose, Emiko Sato, Takefumi Mori, Kiyomi Kisu, Mayuko Ishikawa, Kazuhito Totsune, Tomonori Ishii, Atsuhiro Ichihara, Genevieve Nguyen, Hiroshi Sato, Sadayoshi Ito

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY　308　(5)　F487-F499　2015/03

DOI： 10.1152/ajprenal.00206.2014 　

ISSN： 1931-857X

eISSN： 1522-1466
A functional (pro)renin receptor is expressed in human lymphocytes and monocytes Peer-reviewed

Kaori Narumi, Takuo Hirose, Emiko Sato, Takefumi Mori, Kiyomi Kisu, Mayuko Ishikawa, Kazuhito Totsune, Tomonori Ishii, Atsuhiro Ichihara, Genevieve Nguyen, Hiroshi Sato, Sadayoshi Ito

American Journal of Physiology - Renal Physiology　308　(5)　F487-F499　2015
Publisher: American Physiological Society
DOI： 10.1152/ajprenal.00206.2014 　

ISSN： 1522-1466 0363-6127
THERAPEUTIC EFFECT OF NICOTINAMIDE ON IgA NEPHROPATHY Peer-reviewed

Fushima Tomofumi, Oe Yuji, Iwamori Saki, Sato Emiko, Suzuki Yusuke, Tomino Yasuhiko, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

NEPHROLOGY　19　146-146　2014/05

ISSN： 1320-5358

eISSN： 1440-1797
A NOVEL AND SENSITIVE ASSAY OF KIDNEY HEME OXYGENASE ACTIVITY Peer-reviewed

Iwamori Saki, Sato Emiko, Yoshinari Kouichi, Mano Nariyasu, Ito Sadayoshi, Sato Hiroshi, Takahashi Nobuyuki

NEPHROLOGY　19　185-185　2014/05

ISSN： 1320-5358

eISSN： 1440-1797
Pathology of glomerular lipidosis Peer-reviewed

Hiroshi Sato, Nobuyuki Takahashi, Emiko Sato, Kiyomi Kisu, Sadayoshi Ito, Takao Saito

CLINICAL AND EXPERIMENTAL NEPHROLOGY　18　(2)　194-196　2014/04

DOI： 10.1007/s10157-013-0882-9 　

ISSN： 1342-1751

eISSN： 1437-7799
Solubleform of (pro) renin receptor is excreted from mesothelial cells to peritoneal dialysis effluent of peritoneal dialysis patients Peer-reviewed

Ikuko Oba, Takefumi Mori, Chika Takahashi, Yusuke Ohsaki, Emiko Sato, Kenji Koizumi, Masahide Furusho, Makiko Chida, Fri Naganuma, Sadayoshi Ito

FASEB JOURNAL　28　(1)　2014/04

ISSN： 0892-6638

eISSN： 1530-6860
腹膜透析におけるカルボニルストレス抑制による腹膜保持メカニズムの解明

大場郁子, 森建文, 大崎雄介, 佐藤恵美子, 中道淑美, 福士武, 宮田敏男, 伊藤貞嘉

日本抗加齢医学会総会プログラム・抄録集　13回　190-190　2013/06
Publisher: (一社)日本抗加齢医学会
Albuminuria indicates the pressure-associated injury of juxtamedullary nephrons and cerebral strain vessels in spontaneously hypertensive stroke-prone rats Peer-reviewed

Tasuku Nagasawa, Takefumi Mori, Yusuke Ohsaki, Yoshimi Yoneki, Qi Guo, Emiko Sato, Ikuko Oba, Sadayoshi Ito

HYPERTENSION RESEARCH　35　(10)　1024-1031　2012/10

DOI： 10.1038/hr.2012.112 　

ISSN： 0916-9636
Role of specific T-type calcium channel blocker R(-) efonidipine in the regulation of renal medullary circulation Peer-reviewed

Chunyan Hu, Takefumi Mori, Yi Lu, Qi Guo, Ying Sun, Yoshimi Yoneki, Yusuke Ohsaki, Takashi Nakamichi, Ikuko Oba, Emiko Sato, Susumu Ogawa, Bryan C. Dickinson, Christopher J. Chang, Toshio Miyata, Hiroshi Sato, Sadayoshi Ito

JOURNAL OF HYPERTENSION　30　(8)　1620-1631　2012/08

DOI： 10.1097/HJH.0b013e3283550e9f 　

ISSN： 0263-6352
Determination of reactive oxygen species generated by phorbol 12-myristate 13-acetate-stimulated oral polymorphonuclear cells from healthy human volunteers without any dental problems Peer-reviewed

Noriko Yaekashiwa, Emiko Sato, Keisuke Nakamura, Atsuo Iwasawa, Akihito Kudo, Taro Kanno, Masahiro Kohno, Yoshimi Niwano

ARCHIVES OF ORAL BIOLOGY　57　(6)　636-641　2012/06

DOI： 10.1016/j.archoralbio.2011.10.020 　

ISSN： 0003-9969

eISSN： 1879-1506
Role of Glyoxalase System on Methylglyoxal Induced Peritoneal Thickeness in Glyoxalase Transgenic Rats Peer-reviewed

Ikuko Ooba, Takefumi Mori, Emiko Sato, Yoshimi Yoneki, Kento Akao, Mayuko Ishikawa, Kiyomi Kisu, Hiroko Ito, Mai Saito, Takashi Nakamichi, Hideyasu Kiyomoto, Mariko Miyazaki, Toshio Miyata, Hiroshi Sato, Sadayoshi Ito

FASEB JOURNAL　26　2012/04

ISSN： 0892-6638
Role of renin-Angiotensin system, oxidative stress and inflammation to the blood pressure control in young subjects Peer-reviewed

Sato Emiko, Mori Takefumi, Nakamichi Yoshimi, Fujiwara Mutsuko, Oba Ikuko, Tanno Mizuho, Ogawa Susumu, Kinouchi Yoshitaka, Sato Hiroshi, Hida Wataru, Ito Sadayoshi

XVI INTERNATIONAL CONGRESS ON NUTRITION AND METABOLISM IN RENAL DISEASE (ICRNM)　53-59　2012
Development of A Novel Technique for in Vivo Angiotensin II by LC/MS/MS Peer-reviewed

Takefumi Mori, Emiko Sato, Ikuko Ooba, Shinsaku Suzuki, Yi Lu, Mayuko Ishikawa, Takaaki Goto, Hiroshi Sato, Tomoyuki Oe, Sadayoshi Ito

HYPERTENSION　58　(5)　E86-E86　2011/11

ISSN： 0194-911X
Urinary Carbonyl Compounds and Oxidative Stress May Predict Hypertension in Obese Young Adult Women Peer-reviewed

Takefumi Mori, Emiko Sato, Akihiro Kawamata, Yoshimi Yoneki, Shigeru Kabayama, Sadayoshi Ito, Wataru Hida

HYPERTENSION　58　(5)　E137-E137　2011/11

ISSN： 0194-911X
Kinetic analysis of reactive oxygen species generated by the in vitro reconstituted NADPH oxidase and xanthine oxidase systems Peer-reviewed

Emiko Sato, Takayuki Mokudai, Yoshimi Niwano, Masahiro Kohno

JOURNAL OF BIOCHEMISTRY　150　(2)　173-181　2011/08

DOI： 10.1093/jb/mvr051 　

ISSN： 0021-924X

eISSN： 1756-2651
Metabolomic analysis of human plasma from haemodialysis patients Peer-reviewed

Emiko Sato, Masahiro Kohno, Masanori Yamamoto, Tatsuya Fujisawa, Kouichi Fujiwara, Noriaki Tanaka

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION　41　(3)　241-255　2011/03

DOI： 10.1111/j.1365-2362.2010.02398.x 　

ISSN： 0014-2972
Impact of the Oral Adsorbent AST-120 on Organ-Specific Accumulation of Uremic Toxins: LC-MS/MS and MS Imaging Techniques Peer-reviewed

Sato E, Saigusa D, Mishima E, Uchida T, Miura D, Morikawa-Ichinose T, Kisu K, Sekimoto A, Saito R, Oe Y, Matsumoto Y, Tomioka Y, Mori T, Takahashi N, Sato H, Abe T, Niwa T, Ito S

Toxins (Basel)　10　(1)　pii: E19　2011
Reevaluation of Quantitative ESR Spin Trapping Analysis of Hydroxyl Radical by Applying Sonolysis of Water as a Model System Peer-reviewed

Keisuke Nakamura, Taro Kanno, Hiroyo Ikai, Emiko Sato, Takayuki Mokudai, Yoshimi Niwano, Toshihiko Ozawa, Masahiro Kohno

BULLETIN OF THE CHEMICAL SOCIETY OF JAPAN　83　(9)　1037-1046　2010/09

DOI： 10.1246/bcsj.20100078 　

ISSN： 0009-2673

eISSN： 1348-0634
Generation of reactive oxygen species from conventional laboratory media Peer-reviewed

Takuji Nakashima, Tamae Seki, Atsuko Matsumoto, Hiromi Miura, Emiko Sato, Yoshimi Niwano, Masahiro Kohno, Satoshi Omura, Yoko Takahashi

JOURNAL OF BIOSCIENCE AND BIOENGINEERING　110　(3)　304-307　2010/09

DOI： 10.1016/j.jbiosc.2010.03.003 　

ISSN： 1389-1723

eISSN： 1347-4421
Evaluation of the potential biological toxicities of aqueous extracts from red tide phytoplankton cultures in in vitro and in vivo systems Peer-reviewed

Daekyung Kim, Seon-Heui Cha, Emiko Sato, Yoshimi Niwano, Masahiro Kohno, Zedong Jiang, Yasuhiro Yamasaki, Yukihiko Matsuyama, Kenichi Yamaguchi, Tatsuya Oda

JOURNAL OF TOXICOLOGICAL SCIENCES　35　(4)　591-599　2010/08

DOI： 10.2131/jts.35.591 　

ISSN： 0388-1350

eISSN： 1880-3989
In vitro and in vivo evaluation of mutagenicity of fucoxanthin (FX) and its metabolite fucoxanthinol (FXOH) Peer-reviewed

Fumiaki Beppu, Yoshimi Niwano, Emiko Sato, Masahiro Kohno, Takayuki Tsukui, Masashi Hosokawa, Kazuo Miyashita

JOURNAL OF TOXICOLOGICAL SCIENCES　34　(6)　693-698　2009/12

DOI： 10.2131/jts.34.693 　

ISSN： 0388-1350

eISSN： 1880-3989
Proposed Mechanisms for HOOOH Formation in Two Typical Enzyme Reactions Responsible for Superoxide Anion Production in Biological Systems Invited Peer-reviewed

Masahiro Kohno, Emiko Sato, Noriko Yaekashiwa, Takayuki Mokudai, Yoshimi Niwano

CHEMISTRY LETTERS　38　(4)　302-307　2009/04

DOI： 10.1246/cl.2009.302 　

ISSN： 0366-7022

eISSN： 1348-0715
ナノマイザー技術を応用した全粒大豆を用いた大豆飲料の開発

島田太一, 別府史章, 庭野吉己, 北川昭夫, 上東亨子, 佐藤恵美子, 河野雅弘

月刊 FOOD STYLE21 食品の機能と健康を考える化学情報誌　13　(3)　86-89　2009/03
Publisher:
ISSN： 1343-9502
Fermented Garlic, a Novel Candidate Food for the Prevention of Diabetic Nephropathy Peer-reviewed

Emiko Sato, Yoshimi Niwano, Masahiro Kohno

FREE RADICAL BIOLOGY AND MEDICINE　47　S89-S89　2009

ISSN： 0891-5849
Reactive Oxygen Species Produced by Human Oral Neutrophils Belongs to Free Radical Species Peer-reviewed

Noriko Yaekashiwa, Emiko Sato, Yoshimi Niwano, Masahiro Kohno

FREE RADICAL BIOLOGY AND MEDICINE　47　S134-S134　2009

ISSN： 0891-5849
Existence of a new reactive intermediate oxygen species in hypoxanthine and xanthine oxidase reaction Peer-reviewed

Emiko Sato, Takayuki Mokudai, Yoshimi Niwano, Masato Kamibayashi, Masahiro Kohno

CHEMICAL & PHARMACEUTICAL BULLETIN　56　(8)　1194-1197　2008/08

DOI： 10.1248/cpb.56.1194 　

ISSN： 0009-2363
Emiko Sato, Takayuki Mokudai, Yoshimi Niwano, Masato Kamibayashi, Masahiro Kohno,* Peer-reviewed

Emiko Sato, Takayuki Mokudai, Yoshimi Niwano, Masato Kamibayashi, Masahiro Kohno, “Existence of a, New, Reactive Intermediate Oxygen, Species in Hypoxanthine, Xanthine Oxidase

Chemical & Pharmaceutical Bulletin　56　1194-1197　2008/05/19
Ciclopirox olamine directly scavenges hydroxyl radical Peer-reviewed

Emiko Sato, Masahiro Kohno, Takuji Nakashima, Yoshimi Niwano

INTERNATIONAL JOURNAL OF DERMATOLOGY　47　(1)　15-18　2008/01

DOI： 10.1111/j.1365-4632.2007.03359.x 　

ISSN： 0011-9059
A prodigiosin analogue inactivates NADPH oxidase in macrophage cells by inhibiting assembly of p47phox and rac Peer-reviewed

Takuji Nakashima, Takashi Iwashita, Tsuyoshi Fujita, Emiko Sato, Yoshimi Niwano, Masahiro Kohno, Shunsuke Kuwahara, Nobuyuki Harada, Satoshi Takeshita, Tatsuya Oda

JOURNAL OF BIOCHEMISTRY　143　(1)　107-115　2008/01

DOI： 10.1093/jb/mvm196 　

ISSN： 0021-924X

eISSN： 1756-2651
Clindamycin phosphate scavenges hydroxyl radical Peer-reviewed

Emiko Sato, Masatoshi Kato, Masahiro Kohno, Yoshimi Niwano

INTERNATIONAL JOURNAL OF DERMATOLOGY　46　(11)　1185-1187　2007/11

DOI： 10.1111/j.1365-4632.2007.03338.x 　

ISSN： 0011-9059
Radical scavenging and singlet oxygen quenching activity of marine carotenoid fucoxanthin and its metabolites Peer-reviewed

Nakkarike M. Sachindra, Emiko Sato, Hayato Maeda, Masashi Hosokawa, Yoshimi Niwano, Masahiro Kohno, Kazuo Miyashita

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY　55　(21)　8516-8522　2007/10

DOI： 10.1021/jf071848a 　

ISSN： 0021-8561

eISSN： 1520-5118
A discrepancy in superoxide scavenging activity between the ESR-spin trapping method and the luminol chemiluminescence method Peer-reviewed

Emiko Sato, Yoshimi Niwano, Takayuki Mokudai, Masahiro Kohno, Yukihiko Matsuyama, Daekyung Kim, Tatsuya Oda

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY　71　(6)　1505-1513　2007/06

DOI： 10.1271/bbb.70011 　

ISSN： 0916-8451

eISSN： 1347-6947
Radical generation by the non-enzymatic reaction of methylglyoxal and hydrogen peroxide Peer-reviewed

Masaaki Nakayama, Keita Saito, Emiko Sato, Keisuke Nakayama, Hiroyuki Terawaki, Sadayoshi Ito, Masahiro Kohno

REDOX REPORT　12　(3)　125-133　2007/06

DOI： 10.1179/135100007X200182 　

ISSN： 1351-0002
Antioxidant properties of aqueous extracts from red tide plankton cultures Peer-reviewed

Yoshimi Niwano, Emiko Sato, Masahiro Kohno, Yukihiko Matsuyama, Daekyung Kim, Tatsuya Oda

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY　71　(5)　1145-1153　2007/05

DOI： 10.1271/bbb.60593 　

ISSN： 0916-8451

eISSN： 1347-6947
Inhibitory or scavenging action of ketoconazole and ciclopiroxolamine against reactive oxygen species released by primed inflammatory cells Peer-reviewed

T. Nakashima, E. Sato, Y. Niwano, M. Kohno, W. Muraoka, T. Oda

BRITISH JOURNAL OF DERMATOLOGY　156　(4)　720-727　2007/04

DOI： 10.1111/j.1365-2133.2006.07655.x 　

ISSN： 0007-0963
Some dinophycean red tide plankton species generate a superoxide scavenging substance Peer-reviewed

Emiko Sato, Yoshimi Niwano, Yukihiko Matsuyama, Daekyung Kim, Takuji Nakashima, Tatsuya Oda, Masahiro Kohno

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY　71　(3)　704-710　2007/03

DOI： 10.1271/bbb.60559 　

ISSN： 0916-8451

eISSN： 1347-6947
Some dinophycean red tide plankton species generate a superoxide scavenging substance Peer-reviewed

Emiko Sato, Yoshinti Niwano, Takayuki Mokudan, Yukihiko Matsuyama, Daekyung Kim, Takuji Nakashima, Tatsuya Oda, Masahiro Kohno

FREE RADICAL BIOLOGY AND MEDICINE　43　(3)　S99-S99　2007

DOI： 10.1271/bbb.60559 　

ISSN： 0891-5849
Increased anti-oxidative potency of garlic by spontaneous short-term fermentation Peer-reviewed

Emiko Sato, Masahiro Kohno, Hamasuke Hamano, Yoshimi Niwano

PLANT FOODS FOR HUMAN NUTRITION　61　(4)　157-160　2006/12

DOI： 10.1007/s11130-006-0017-5 　

ISSN： 0921-9668
Increased level of tetrahydro-beta-carboline derivatives in short-term fermented garlic Peer-reviewed

Emiko Sato, Masahiro Kohno, Yoshimi Niwano

PLANT FOODS FOR HUMAN NUTRITION　61　(4)　175-178　2006/12

DOI： 10.1007/s11130-006-0028-2 　

ISSN： 0921-9668
Spectroscopic and DNA-binding characterization of the isolated heme-bound basic helix-loop-helix-PAS-A domain of neuronal PAS protein 2 (NPAS2), a transcription activator protein associated with circadian rhythms Peer-reviewed

Y Mukaiyama, T Uchida, E Sato, A Sasaki, Y Sato, J Igarashi, H Kurokawa, Sagami, I, T Kitagawa, T Shimizu

FEBS JOURNAL　273　(11)　2528-2539　2006/06

DOI： 10.1111/j.1742-4658.2006.05259.x 　

ISSN： 1742-464X
生にんにくと熟成醗酵黒にんにくの抗酸化能の比較 Peer-reviewed

佐藤恵美子, 河野雅弘, 庭野吉己

日本栄養・食糧学会大会講演要旨集　60回　194-194　2006/04
Publisher: (公社)日本栄養・食糧学会
マクロファージと植物プランクトンにおけるスーパーオキシド生成に対するγ-proteobacteriumにより産生されるprodigiosinの効果(Effect of prodigiosin produced by γ-proteobacterium on superoxide generation in macrophage and phytoplankton)

Nakashima Takuji, Kim Daekyung, Sato Emiko, Miyazaki Yousuke, Kurachi Maki, Yanaguchi Kenichi, Niwano Yoshimi, Oda Tatsuya

生化学　77　(8)　824-824　2005/08
Publisher: (公社)日本生化学会
ISSN： 0037-1017
Spectroscopic characterization of the isolated heme-bound PAS-B domain of neuronal PAS domain protein 2 associated with circadian rhythms Peer-reviewed

R Koudo, H Kurokawa, E Sato, J Igarashi, T Uchida, Sagami, I, T Kitagawa, T Shimizu

FEBS JOURNAL　272　(16)　4153-4162　2005/08

DOI： 10.1111/j.1742-4658.2005.04828.x 　

ISSN： 1742-464X
CO-dependent activity-controlling mechanism of heme-containing CO-sensor protein, neuronal PAS domain protein Peer-reviewed

T Uchida, E Sato, A Sato, Sagami, I, T Shimizu, T Kitagawa

JOURNAL OF BIOLOGICAL CHEMISTRY　280　(22)　21358-21368　2005/06

DOI： 10.1074/jbc.M412350200 　

ISSN： 0021-9258
SOUL in mouse eyes is a new hexameric heme-binding protein with characteristic optical absorption, resonance Raman spectral, and heme-binding properties Peer-reviewed

E Sato, Sagami, I, T Uchida, A Sato, T Kitagawa, J Igarashi, T Shimizu

BIOCHEMISTRY　43　(44)　14189-14198　2004/11

DOI： 10.1021/bi048742i 　

ISSN： 0006-2960

Show all ︎Show first 5

Misc. 177

臨床に資するバイオプシー研究最前線メタボロミクスから紐解く低出生体重が及ぼす将来の妊娠への影響モデルマウスを用いた肝臓と胎盤の評価

佐藤恵美子

JSBMS Letters　49　(Suppl.)　40-40　2024/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
慢性腎臓病の早期診断法確立を目指した硫黄代謝物に基づく呼気オミックス

逸見佳宣, 緒方星陵, 高田剛, 三枝大輔, 三巻英換, 魏范研, 赤池孝章, 佐藤恵美子

JSBMS Letters　49　(Suppl.)　111-111　2024/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
慢性腎臓病のウレミックサルコペニアにおけるマイオカインの効果

山越聖子, 高橋知香, 森建文, 佐藤恵美子

日本腎臓学会誌　66　(4)　580-580　2024/06
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
慢性腎臓病の早期診断法確立を目指した硫黄代謝物に基づく呼気オミックス

逸見佳宣, 緒方星陵, 井田智章, 三枝大輔, 三島英換, 高橋信行, 魏范研, 赤池孝章, 佐藤恵美子

日本腎臓学会誌　66　(4)　632-632　2024/06
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
中性4.25%ブドウ糖腹膜透析液の除水特性と安全性

森建文, 矢花郁子, 石山勝也, 橋本英明, 中山晋吾, 伊藤大樹, 鎌田綾佳, 遠藤明里, 佐藤恵美子, 木村朋由

日本透析医学会雑誌　57　(Suppl.1)　542-542　2024/05
Publisher: (一社)日本透析医学会
ISSN： 1340-3451

eISSN： 1883-082X
Effects of low birthweight on blood pressure, renal development, and the next generation and study of their treatment

佐藤恵美子, 佐藤恵美子, 堰本晃代, 山越聖子, 伏木由衣, 三枝大輔, 高橋信行, 高橋信行, 三島英換

日本高血圧学会総会プログラム・抄録集(CD-ROM)　46th　2024
Investigation of preventive methods for tissue aging targeting uremic toxin induced intracellular metabolic changes

佐藤恵美子

代謝異常治療研究基金研究業績集　47　2024

ISSN： 0388-5224
慢性腎臓病(CKD)における硫黄代謝物に基づく呼気オミックス

逸見佳宣, 緒方星陵, 井田智章, 三枝大輔, 魏范研, 赤池孝章, 佐藤恵美子

JSBMS Letters　48　(Suppl.)　63-63　2023/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
尿毒素と筋肉減少病態,運動療法の腎保護のエビデンス

佐藤恵美子, 佐藤恵美子, 山越聖子

日本腎臓リハビリテーション学会学術集会プログラム・抄録集　13th　2023
慢性腎不全時のサルコペニアの病態の基礎

佐藤恵美子

日本腎臓リハビリテーション学会誌　1　(2)　260-273　2022/11
Publisher: (一社)日本腎臓リハビリテーション学会
ISSN： 2436-8180

eISSN： 2436-8253
腎不全モデルマウスの血漿および筋・腎・肝組織の代謝物解析

逸見佳宣, 木村有那, 三枝大輔, 佐藤恵美子

JSBMS Letters　47　(Suppl.)　111-111　2022/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
【腎疾患におけるサルコペニア・フレイルの病態と臨床】慢性腎臓病におけるサルコペニア・フレイルの発症機序-尿毒素、腸内細菌環境悪化、慢性炎症とミトコンドリア機能不全

鈴木健弘, 佐藤恵美子, 阿部高明

腎臓内科　16　(1)　22-30　2022/07
Publisher: (有)科学評論社
ISSN： 2435-1903
サルコペニア・フレイルと尿毒素吸着薬

佐藤恵美子

腎臓内科　16　(1)　94-99　2022/07
Publisher: (有)科学評論社
ISSN： 2435-1903
ラクトフェリン投与による慢性腎臓病およびその合併症の進行抑制効果

岩本千奈, 堰本晃代, 高橋信行, 佐藤恵美子

日本腎臓学会誌　64　(3)　221-221　2022/05
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
尿毒素曝露下の筋細胞におけるマイオカインの影響

山越聖子, 佐藤恵美子, 高橋知香, 伊藤大樹, 遠藤明里, 矢花郁子, 阿南剛, 広瀬卓男, 木村朋由, 森建文

日本腎臓学会誌　64　(3)　221-221　2022/05
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
糖尿病における腎機能変化とシトルリン・アルギニン・オルニチン変化の関連

小川晋, 清水麻那美, 佐藤恵美子

糖尿病　65　(Suppl.1)　S-182　2022/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
低出生体重が及ぼす将来の妊娠への影響モデルマウスを用いた胎仔および胎盤の評価

山本真莉, 堰本晃代, 大川雅敬, 高橋信行, 佐藤恵美子

DOHad研究(Web)　10　(2)　2022

ISSN： 2187-2597
低出生体重が及ぼす将来の妊娠への影響モデルマウスを用いた母体の評価

大川雅敬, 堰本晃代, 山本真莉, 高橋信行, 佐藤恵美子

DOHad研究(Web)　10　(2)　2022

ISSN： 2187-2597
Tadalafil投与が子宮灌流圧低下マウスの仔の出生体重と腎発達不全に与える影響

猿山春花, 堰本晃代, 高相陽子, 高橋信行, 佐藤恵美子

DOHad研究(Web)　10　(2)　2022

ISSN： 2187-2597
ラクトフェリン投与による慢性腎臓病およびその合併症の進行抑制効果

岩本千奈, 堰本晃代, 高橋信行, 佐藤恵美子

日本腎臓学会誌(Web)　64　(3)　2022

ISSN： 1884-0728
凝固活性と関連する尿毒素の網羅的検討

山陰周, 大江佑治, 佐藤恵美子, 堰本晃代, 宮崎真理子, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　63　(4)　458-458　2021/06
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
ウレミックトキシンが凝固線溶系因子発現に及ぼす影響

大江佑治, 佐藤恵美子, 佐藤博, 宮崎真理子, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　63　(4)　510-510　2021/06
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
Evaluation of intracellular metabolic alteration in uremic toxin exposure neurons and renal failure mouse brain

佐藤恵美子, 佐藤恵美子, 渡辺真由, 熊倉慧, 高橋信行, 高橋信行

JSBMS Letters　46　(Supplement)　2021

ISSN： 1881-5464
Evaluation of the effect of Methylglyoxal on metabolic alternation in myoblast cells

細田祐衣, 渡辺真由, 堰本晃代, 高橋信行, 佐藤恵美子

JSBMS Letters　46　(Supplement)　2021

ISSN： 1881-5464
CKDにおける腸内環境不全時の尿毒素蓄積とサルコペニア

佐藤恵美子, 佐藤恵美子

日本腎臓リハビリテーション学会学術集会プログラム・抄録集　11th　2021
ウレミックトキシンが凝固線溶系因子発現に及ぼす影響

大江佑治, 佐藤恵美子, 佐藤博, 宮崎真理子, 伊藤貞嘉, 高橋信行

日本腎臓学会誌(Web)　63　(4)　2021

ISSN： 1884-0728
The effects of adsorbent on intestinal dysbiosis and sarcopenia in CKD

佐藤恵美子, 阿部高明

腎と透析　90　(3)　2021

ISSN： 0385-2156
【腎臓リハビリテーション】尿毒素による筋萎縮メカニズム

佐藤恵美子, 阿部高明

日本腎臓学会誌　62　(7)　757-762　2020/10
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
Effects of the oral adsorbent AST-120 on fecal p-cresol and indole levels and on the gut microbiota composition. International-journal

Emiko Sato, Koji Hosomi, Akiyo Sekimoto, Eikan Mishima, Yuji Oe, Daisuke Saigusa, Sadayoshi Ito, Takaaki Abe, Hiroshi Sato, Jun Kunisawa, Toshimitsu Niwa, Nobuyuki Takahashi

Biochemical and biophysical research communications　525　(3)　773-779　2020/05/07

DOI： 10.1016/j.bbrc.2020.02.141 　

More details Close

In chronic kidney disease, elevated levels of circulating uremic toxins are associated with a variety of symptoms and organ dysfunction. Indoxyl sulfate (IS) and p-cresyl sulfate (pCS) are microbiota-derived metabolites and representative uremic toxins. We have previously shown that the oral adsorbent AST-120 profoundly reduced pCS compared to IS in adenine-induced renal failure in mice. However, the mechanisms of the different attenuation effects of AST-120 between IS and pCS are unclear. To clarify the difference of AST-120 on IS and pCS, we investigated the levels of fecal indole and p-cresol, the respective precursors of IS and pCS, and examined the influence on the gut microbiota. Although fecal indole was detected in all groups analyzed, fecal p-cresol was not detected in AST-120 treatment groups. In genus level, a total of 23 organisms were significantly changed by renal failure or AST-120 treatment. Especially, AST-120 reduced the abundance of Erysipelotrichaceae uncultured and Clostridium sensu stricto 1, which have a gene involved in p-cresol production. Our findings suggest that, in addition to the adsorption of the uremic toxin precursors, AST-120 affects the abundance of some gut microbiota in normal and renal failure conditions, thereby explaining the different attenuation effects on IS and pCS.
ニコチンアミドは炎症の抑制によりアデニン腎症発生を予防する.

熊倉慧, 佐藤恵美子, 堰本晃代, 大江佑治, 宮崎真理子, 高橋信行

日本腎臓学会誌(Web)　62　(4)　2020

ISSN： 1884-0728
単球・マクロファージ由来組織因子の慢性腎臓病における役割

山陰周, 大江佑治, 佐藤恵美子, 堰本晃代, 岡本好司, 宮崎真理子, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌(Web)　62　(4)　2020

ISSN： 1884-0728
Mechanisms of uremic toxins-induced uremic sarcopenia

佐藤恵美子, 佐藤恵美子, 阿部高明, 阿部高明, 阿部高明

日本腎臓学会誌(Web)　62　(7)　2020

ISSN： 1884-0728
内皮型NO合成酵素欠損はCKD関連異所性石灰化を誘導する

大江佑治, 佐藤恵美子, 宮崎真理子, 岡本好司, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌(Web)　62　(4)　2020

ISSN： 1884-0728
抗HIV/HBV薬テノホビルジソプロキシルフマル酸塩関連腎障害の病態解明及び予防法の検討

佐藤恵美子

医科学応用研究財団研究報告(CD-ROM)　37　2020

ISSN： 2185-2561
カルボニルストレス誘導筋細胞内代謝変化のGC-MSによる評価

佐藤恵美子, 佐藤恵美子, 等々力崇太, 山本多恵, 宮崎真理子, 森建文, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

JSBMS Letters　44　(Supplement)　2019

ISSN： 1881-5464
既存薬スクリーニングによる抗フェロトーシス薬の同定と急性腎障害保護効果の検討

三島英換, 佐藤恵美子, 鈴木健弘, 伊藤貞嘉, 阿部高明

日本腎臓学会誌　61　(3)　2019

ISSN： 0385-2385
肥満に対するアルドステロンの影響-小腸におけるグルコース吸収の役割-

白井英和, 内田多恵子, 橋爪大和, 大屋咲子, 堰本晃代, 大江佑治, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集(CD-ROM)　42nd　2019
腎不全マウスの腸内細菌叢と腸内腐敗物の変化とAST-120による影響

佐藤恵美子, 細見晃司, 三枝大輔, 堰本晃代, 國澤純, 丹羽利充, 佐藤博, 高橋信行

JSBMS Letters　43　(Suppl.)　98-98　2018/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
腎不全マウスの腸内細菌叢と腸内腐敗物の変化とAST‐120による影響

佐藤恵美子, 細見晃司, 三枝大輔, 堰本晃代, 國澤純, 丹羽利充, 佐藤博, 高橋信行

JSBMS Letters　43　(Suppl.)　98-98　2018/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
Protease‐Activated receptor(PAR2)のCKDにおける役割

佐藤恵美子, 高橋信行

宮城県腎臓協会会報　(29)　83　2018/07/31

ISSN： 2432-3101
sFlt-1過剰発現妊娠高血圧腎症モデルマウスでアシルカルニチンが上昇する機序

佐藤恵美子, 金子茉那美, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　60　(3)　334-334　2018/04
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385
血液凝固系に関連した糖尿病性腎症早期診断・薬効マーカー

佐藤恵美子, 大江佑治, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　60　(3)　402-402　2018/04
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385
抗HIV/HBV薬テノホビルジソプロキシルフマル酸塩関連腎障害の病態解明及び予防法の検討—助成課題生活習慣病における医学,薬学の萌芽的研究

佐藤恵美子

医科学応用研究財団研究報告 / 鈴木謙三記念医科学応用研究財団 [編]　37　289-292　2018
Publisher: 鈴木謙三記念医科学応用研究財団
ISSN： 0914-5117
メタボロミクスによるsFlt-1過剰発現妊娠高血圧腎症モデルでアシルカルニチンが上昇する機序の解明

佐藤恵美子, 佐藤恵美子, 金子茉那美, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 堰本晃代, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本妊娠高血圧学会雑誌　25　2018

ISSN： 1880-3172
慢性腎臓病における尿毒素物質によるエイジング

森建文, 佐藤恵美子, 矢花郁子, 室谷嘉一, 室谷嘉一, 伊藤修, 伊藤貞嘉

日本腎臓リハビリテーション学会学術集会プログラム・抄録集　8th　98　2018
血液凝固系に関連した糖尿病性腎症早期診断・薬効マーカー

佐藤恵美子, 大江佑治, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　60　(3)　402　2018

ISSN： 0385-2385
腎うっ血による腎障害機序の解明

島田佐登志, 大崎雄介, 高橋知香, 廣瀬卓男, 佐藤恵美子, 伊藤貞嘉, 森建文

日本腎臓学会誌　60　(3)　334　2018

ISSN： 0385-2385
sFlt‐1過剰発現妊娠高血圧腎症モデルマウスでアシルカルニチンが上昇する機序

佐藤恵美子, 金子茉那美, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　60　(3)　334　2018

ISSN： 0385-2385
Reduced Uterine Perfusion Pressure(RUPP)preeclampsia(PE)モデルにおけるマウス系統および術式の検討

堰本晃代, 堰本晃代, 伏間智史, 大江佑治, 佐藤恵美子, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　40th　362　2017/10/20
sFlt‐1過剰発現eNOS欠損マウスは重症肝障害と血小板減少症を発症する

大江佑治, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　40th　362-362　2017/10/20
Publisher: (NPO)日本高血圧学会
腎不全におけるサルコペニア

佐藤恵美子

循環器内科　82　(4)　358-364　2017/10
Publisher: (有)科学評論社
ISSN： 1884-2909
腎臓とグアニジノ化合物 4)腹膜透析とグアニジノ化合物

佐藤恵美子, 佐藤恵美子, 森建文

腎と透析　83　46‐50　2017/09/30

ISSN： 0385-2156
sFlt‐1過剰発現eNOS欠損マウスは重症肝障害と血小板減少症を発症する

大江佑治, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行, 高橋信行

日本妊娠高血圧学会雑誌　24　60-60　2017/09
Publisher: (一社)日本妊娠高血圧学会
ISSN： 1880-3172
RUPP PEモデルにおけるマウス系統および術式の検討

堰本晃代, 堰本晃代, 伏間智史, 大江佑治, 佐藤恵美子, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本妊娠高血圧学会雑誌　24　73　2017/09

ISSN： 1880-3172
【尿毒症とグアニジノ化合物-機能性小分子研究の歴史と新たな展開-】腎臓とグアニジノ化合物腹膜透析とグアニジノ化合物

佐藤恵美子, 森建文

腎と透析　83　(別冊尿毒症とグアニジノ化合物-機能性小分子研究の歴史と新たな展開-)　46-50　2017/09
Publisher: (株)東京医学社
ISSN： 0385-2156
LC‐MS/MSとイメージングMSによる腎不全時における尿毒素臓器蓄積とAST‐120による治療効果の評価

佐藤恵美子, 佐藤恵美子, 三枝大輔, 三島英換, 三浦大典, 佐藤博, 佐藤博, 丹羽利充, 伊藤貞嘉

JSBMS Letters　42　(Supplement)　97-97　2017/08/25
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
LC-MS/MSとイメージングMSによる腎不全時における尿毒素臓器蓄積とAST-120による治療効果の評価

佐藤恵美子, 三枝大輔, 三島英換, 三浦大典, 佐藤博, 丹羽利充, 伊藤貞嘉

JSBMS Letters　42　(Suppl.)　97-97　2017/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
腹膜中皮細胞におけるNrf2システムの役割

矢花郁子, 高橋知香, 大崎雄介, 佐藤恵美子, 伊藤貞嘉, 森建文

日本透析医学会雑誌　50　(Supplement 1)　770-770　2017/05/28
Publisher: (一社)日本透析医学会
ISSN： 1340-3451

eISSN： 1883-082X
腎不全時における全身臓器での尿毒素蓄積とAST‐120による蓄積軽減効果

佐藤恵美子, 三島英換, 三枝大輔, 内田多恵子, 高橋信行, 佐藤博, 丹羽利充, 森建文, 伊藤貞嘉

日本腎臓学会誌　59　(3)　283-283　2017/04/25
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
新規Reduced Uterine Perfusion Pressure(RUPP)PEモデルの開発におけるマウス系統の重要性

堰本晃代, 伏間智史, 大江佑治, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　59　(3)　304　2017/04/25

ISSN： 0385-2385
ニコチンアミドによる妊娠高血圧腎症治療におけるCD38の役割

高橋信行, 石田晃規, 伏間智史, 増島直弥, 堰本晃代, 佐藤恵美子, 佐藤博, 伊藤貞嘉

日本腎臓学会誌　59　(3)　233　2017/04/25

ISSN： 0385-2385
妊娠高血圧腎症モデルマウスにおけるプロテアーゼ活性化受容体2の役割

小畑裕史, 江美恵子, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　59　(3)　305　2017/04/25

ISSN： 0385-2385
長時間透析施行中の末梢単核球細胞(PBMCs)におけるNrf2標的遺伝子群およびインドキシル硫酸の変動

鳥越暁, 佐藤恵美子, 山本多恵, 高橋知香, 宮崎真理子, 家入伯夫, 堀田修, 森建文, 伊藤貞嘉

日本腎臓学会誌　59　(3)　347　2017/04/25

ISSN： 0385-2385
上皮‐内皮クロストーク機構の破綻と肝腎障害の新規メカニズム

大江佑治, 伏間智史, 佐藤恵美子, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　59　(3)　230-230　2017/04/25
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
ニコチンアミドによるIgA腎症合併妊娠への治療効果

伏間智史, 堰本晃代, 大江佑治, 佐藤恵美子, 鈴木祐介, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　59　(3)　305　2017/04/25

ISSN： 0385-2385
腎不全時における全身臓器での尿毒素蓄積とAST-120による蓄積軽減効果

佐藤恵美子, 三島英換, 三枝大輔, 内田多恵子, 高橋信行, 佐藤博, 丹羽利充, 森建文, 伊藤貞嘉

日本腎臓学会誌　59　(3)　283-283　2017/04
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
尿毒素による細胞内代謝変化は慢性腎臓病においてサルコペニアを引き起こす

佐藤恵美子, 三島英換, 森建文, 鈴木亜里沙, 三枝大輔, 高橋信行, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本薬学会年会要旨集　137年会　(4)　89-89　2017/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
メタボロミクスによるsFlt-1過剰発現妊娠高血圧腎症モデルマウスの病態解析

金子茉那美, 佐藤恵美子, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 高橋信行

日本薬学会年会要旨集　137年会　(4)　89-89　2017/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
カテキンの光酸化を介した殺菌活性と光酸化機序の解明

宍戸駿一, 宮野怜, 中島琢自, 中島琢自, 佐藤恵美子, 中村圭祐, 菅野太郎, 江草宏, 庭野吉己

日本防菌防黴学会年次大会要旨集　44th　2017
尿毒素による細胞内代謝変化は慢性腎臓病においてサルコペニアを引き起こす

佐藤恵美子, 佐藤恵美子, 三島英換, 森建文, 鈴木亜里沙, 三枝大輔, 高橋信行, 高橋信行, 佐藤博, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本薬学会年会要旨集(CD-ROM)　137th　(4)　ROMBUNNO.27I‐am10-89　2017
Publisher: (公社)日本薬学会
ISSN： 0918-9823
慢性腎臓病におけるプロテアーゼ活性化受容体2の役割

林咲貴子, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉, 高橋信行, 高橋信行

日本薬学会年会要旨集(CD-ROM)　137th　ROMBUNNO.27I‐am13S　2017
住民健診における尿中アンジオテンシノージェンとカルボニル物質排泄量は高血圧に関与する

森建文, 森建文, 佐藤恵美子, 王安邑, 伊藤貞嘉

日本抗加齢医学会総会プログラム・抄録集　17th　186　2017
妊娠高血圧腎症の新規薬物治療

高橋信行, 高橋信行, 伏間智史, 大柳元, 佐藤恵美子, 佐藤恵美子, 中田宏伸, 大江佑治, 堰本晃代, 堰本晃代, 三枝大輔, 佐藤博, 佐藤博, 伊藤貞嘉, LI Feng, JENNETTE JC, 前田信代, KARUMANCHI Ananth, SMITHIES Oliver

日本薬学会年会要旨集(CD-ROM)　137th　(4)　ROMBUNNO.25F‐pm16-57　2017
Publisher: (公社)日本薬学会
ISSN： 0918-9823
メタボロミクスによるsFlt‐1過剰発現妊娠高血圧腎症モデルマウスの病態解析

金子茉那美, 佐藤恵美子, 佐藤恵美子, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本薬学会年会要旨集(CD-ROM)　137th　ROMBUNNO.27I‐am11S　2017
アデニン腎症におけるプロテアーゼ活性化受容体2の役割

林咲貴子, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　59　(3)　290　2017

ISSN： 0385-2385
新規全身性エリテマトーデス合併妊娠高血圧腎症モデルマウスの作製

伊丸岡健太, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　59　(3)　360　2017

ISSN： 0385-2385
(プロ)レニンレセプターを介したインドキシル硫酸の蓄積によるメサンギウム領域の拡大・線維化の検討

鳴海かほり, 佐藤恵美子, 山本多恵, 宮崎真理子, 佐藤博, 伊藤貞嘉

日本腎臓学会誌　59　(3)　302　2017

ISSN： 0385-2385
メタボロミクスによるsFlt‐1過剰発現妊娠高血圧腎症モデルマウスの病態解析

金子茉那美, 佐藤恵美子, 津國由佳子, 伏間智史, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　59　(3)　230　2017

ISSN： 0385-2385
新規全身性エリテマトーデス合併妊娠高血圧腎症モデルマウスの開発

大江佑治, 大江佑治, 伊丸岡健太, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行, 高橋信行

日本妊娠高血圧学会雑誌　24　74　2017

ISSN： 1880-3172
新規全身性エリテマトーデス合併妊娠高血圧腎症モデルマウスの開発

伊丸岡健太, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 菅原準一, 伊藤貞嘉, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　40th　362　2017
腎不全におけるサルコペニア

佐藤恵美子

循環器内科　82　(4)　358‐364　2017

ISSN： 1884-2909
未知の脂肪細胞由来アルドステロン合成酵素(CYP11B2)発現誘導因子の探索

島田洋樹, 伊藤亮, 佐藤恵美子, 伊藤貞嘉, 横山敦, 菅原明

日本高血圧学会総会プログラム・抄録集　39th　331-331　2016/09/30
Publisher: (NPO)日本高血圧学会
メタボロミクスによるsFlt‐1過剰発現妊娠高血圧腎症モデルマウスの病態解析

佐藤恵美子, 佐藤恵美子, 津國由佳子, 伏間智史, 金子茉那美, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　324　2016/09/30
LPS投与妊娠高血圧腎症モデルマウスにおけるプロテアーゼ活性化受容体2の役割

江美恵子, 小畑裕史, 大江佑治, 大江佑治, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　325　2016/09/30
CKDにおけるサルコペニアの発症機序の解明

佐藤恵美子, 佐藤恵美子, 森建文, 三島英換, 鈴木亜里沙, 高橋信行, 高橋信行, 佐藤博, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　39th　329　2016/09/30
新規Reduced Uterine Perfusion Pressure(RUPP)マウスモデルの開発

伏間智史, 堰本晃代, 堰本晃代, 大江佑治, 佐藤恵美子, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　325　2016/09/30
C57BL/6Jマウスでの新規Reduced Uterine Perfusion Pressure(RUPP)モデルの開発

堰本晃代, 堰本晃代, 伏間智史, 大江佑治, 大江佑治, 佐藤恵美子, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　342　2016/09/30
eNOS欠損糖尿病性腎症モデルマウスにおける血液凝固第Xa因子‐プロテアーゼ活性化受容体2の役割

大江佑治, 林咲貴子, 伏間智史, 佐藤恵美子, 佐藤恵美子, 金須清美, 佐藤博, 佐藤博, 伊藤貞嘉, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　325　2016/09/30
IgA腎症は妊娠により増悪し,妊娠高血圧腎症の危険因子となる

伏間智史, 大江佑治, 佐藤恵美子, 佐藤恵美子, 鈴木祐介, 富野康日己, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本高血圧学会総会プログラム・抄録集　39th　342　2016/09/30
C57BL/6Jマウスでの新規Reduced Uterine Perfusion Pressure(RUPP)モデルの開発

伏間智史, 堰本晃代, 大江佑治, 佐藤恵美子, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 佐藤博, 高橋信行, 高橋信行

日本妊娠高血圧学会雑誌　23　68　2016/09

ISSN： 1880-3172
メタボロミクスによるsFlt-1過剰発現妊娠高血圧腎症モデルマウスの病態解析

佐藤恵美子, 津國由佳子, 伏間智史, 金子茉那美, 三枝大輔, 堰本晃代, 伊藤貞嘉, 佐藤博, 高橋信行

日本高血圧学会総会プログラム・抄録集　39回　324-324　2016/09
Publisher: (NPO)日本高血圧学会
CKDにおけるサルコペニアの発症機序の解明

佐藤恵美子, 森建文, 三島英換, 鈴木亜里沙, 高橋信行, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　39回　329-329　2016/09
Publisher: (NPO)日本高血圧学会
筋細胞における尿毒素性酸化ストレスは代謝変化を引き起こしサルコペニアの原因となる

佐藤恵美子, 佐藤恵美子, 森建文, 三島英換, 鈴木亜里沙, 庭野吉己, 高橋信行, 高橋信行, 佐藤博, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本酸化ストレス学会学術集会プログラム・抄録集　69th　126　2016/08/30
腹膜透析治療中腎不全患者におけるグアニジノ化合物の意義

佐藤恵美子, 佐藤恵美子

東北医学雑誌　128　(1)　70　2016/06/25

ISSN： 0040-8700
長時間透析と通常透析の末梢単核球細胞におけるNrf2酸化ストレス応答系およびアミノ酸の比較

鳥越暁, 森建文, 佐藤恵美子, 家入伯夫, 高橋知香, 石田洋子, 堀田修, 伊藤貞嘉

日本透析医学会雑誌　49　(Supplement 1)　471　2016/05/28

ISSN： 1340-3451
新規Reduced Uterine Perfusion Pressure(RUPP)マウスモデルの開発

伏間智史, 堰本晃代, 大江佑治, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　58　(3)　303　2016/05/10

ISSN： 0385-2385
メサンギウム増殖性糸球体腎炎患者において血清中可溶型(プロ)レニンレセプターは糸球体硬化度と関連する

鳴海かほり, 佐藤恵美子, 山本多恵, 宮崎真理子, 佐藤博, 伊藤貞嘉

日本腎臓学会誌　58　(3)　298　2016/05/10

ISSN： 0385-2385
インドキシル硫酸によるウレミックサルコペニア発症機序解明

佐藤恵美子, 森建文, 三島英換, 鈴木亜里沙, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本腎臓学会誌　58　(3)　315　2016/05/10

ISSN： 0385-2385
ヒト腹膜中皮細胞の線維化における酸性オルガネラの機能解析

矢花郁子, 森建文, 高橋知香, 大崎雄介, 佐藤恵美子, 伊藤貞嘉

日本腎臓学会誌　58　(3)　258-258　2016/05/10
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
インドキシル硫酸によるウレミックサルコペニア発症機序解明

佐藤恵美子, 森建文, 三島英換, 鈴木亜里沙, 佐藤博, 丹羽利充, 阿部高明, 伊藤貞嘉

日本腎臓学会誌　58　(3)　315-315　2016/05
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385
腎保護薬update 前臨床段階の薬剤グリコシル化阻害薬

森建文, 佐藤恵美子, 大崎雄介, 伊藤貞嘉

腎と透析　80　(4)　547‐550-550　2016/04/25
Publisher: (株)東京医学社
ISSN： 0385-2156
ニコチンアミドがPEに伴うFGRを改善する機序

高橋信行, 高橋信行, 伏間智史, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉

日本妊娠高血圧学会雑誌　23　2016

ISSN： 1880-3172
ニコチンアミドの妊娠高血圧腎症治療効果におけるヘムオキシゲナーゼの役割

高橋信行, 高橋信行, 中田宏伸, 伏間智史, 堰本晃代, 堰本晃代, 大江佑治, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉

日本妊娠高血圧学会雑誌　23　67　2016

ISSN： 1880-3172
メタボローム解析による妊娠高血圧腎症治療標的分子の探索

津國由佳子, 佐藤恵美子, 佐藤恵美子, 伏間智史, 佐藤博, 佐藤博, 高橋信行, 高橋信行, 三枝大輔, 三枝大輔

JSBMS Lett　40　(Supplement)　73-73　2015/08/20
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
インドキシル硫酸は残存腎機能の低下とともに血中に蓄積しウレミックサルコペニアに関係する

佐藤恵美子, 佐藤恵美子, 森建文, 鈴木亜里沙, 菅原真恵, 倉澤奈穂, 三枝大輔, 大場郁子, 永沼絵理, 佐藤博, 佐藤博, 丹羽利充, 伊藤貞嘉

JSBMS Letters　40　(Supplement)　63-63　2015/08/20
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
高齢者の腹膜透析と在宅医療連携

森建文, 矢花郁子, 佐藤真一, 小泉賢治, 千田真貴子, 永沼絵理, 倉澤奈穂, 土川未歩子, 大崎雄介, 佐藤恵美子, 高橋知香, 伊藤貞嘉

東北腎不全研究会誌　25　(1)　80-83　2015/08

ISSN： 0919-3847
ニコチンアミドはAsb4欠損マウスのPE,妊娠の維持,およびに胎児生存率を改善する

高橋信行, 伏間智史, LI Feng, 大江佑治, 佐藤恵美子, 佐藤博, 伊藤貞嘉

日本妊娠高血圧学会雑誌　22　72　2015/08

ISSN： 1880-3172
妊娠高血圧腎症におけるカルニチン代謝の変化

津國由佳子, 佐藤恵美子, 内田多恵子, 伏間智史, 三枝大輔, 佐藤博, 高橋信行

日本妊娠高血圧学会雑誌　22　72-72　2015/08
Publisher: (一社)日本妊娠高血圧学会
ISSN： 1880-3172
新規Reduced Uterine Perfusion Pressure(RUPP)マウスモデルの開発

伏間智史, 堰本晃代, 大江祐治, 金子茉那美, 佐藤恵美子, 伊藤貞嘉, 佐藤博, 高橋信行

日本妊娠高血圧学会雑誌　22　73　2015/08

ISSN： 1880-3172
IgA腎症は妊娠予後を悪化させ,妊娠はIgA腎症を悪化させる(マウスモデルでの検討)

伏間智史, 大江佑治, 佐藤恵美子, 鈴木祐介, 富野康日己, 伊藤貞嘉, 佐藤博, 高橋信行

日本妊娠高血圧学会雑誌　22　73　2015/08

ISSN： 1880-3172
インドキシル硫酸は残存腎機能の低下とともに血中に蓄積しウレミックサルコペニアに関係する

佐藤恵美子, 森建文, 鈴木亜里沙, 菅原真恵, 倉澤奈穂, 三枝大輔, 大場郁子, 永沼絵理, 佐藤博, 丹羽利充, 伊藤貞嘉

JSBMS Letters　40　(Suppl.)　63-63　2015/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
メタボローム解析による妊娠高血圧腎症治療標的分子の探索

津國由佳子, 佐藤恵美子, 伏間智史, 佐藤博, 高橋信行, 三枝大輔

JSBMS Letters　40　(Suppl.)　73-73　2015/08
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
2型糖尿病肥満モデルラットにおける長期的運動の腎NOS蛋白発現への影響

伊藤大亮, 伊藤大亮, 曹鵬宇, 柿花隆昭, 佐藤恵美子, 須田千尋, 坂田佳子, 伊藤修, 上月正博, 清元秀泰

日本NO学会学術集会プログラム抄録集　15th　60　2015/06/12
IgA腎症は妊娠予後を悪化させ,妊娠はIgA腎症を悪化させる(マウスモデルにおける検討)

伏間智史, 大江佑治, 佐藤恵美子, 鈴木祐介, 富野康日己, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　57　(3)　503　2015/04/30

ISSN： 0385-2385
2型糖尿病肥満モデルラットにおける長期的運動の腎NO合成酵素および酸化ストレス系への影響

伊藤大亮, 曹鵬宇, 柿花隆昭, 須田千尋, 佐藤恵美子, 坂田佳子, 伊藤修, 上月正博, 清元秀泰

日本腎臓学会誌　57　(3)　459-459　2015/04/30
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
ヒト免疫細胞に発現する(プロ)レニン受容体の機能検討

鳴海かほり, 廣瀬卓男, 佐藤恵美子, 佐藤博, 森建文, 伊藤貞嘉

日本腎臓学会誌　57　(3)　594　2015/04/30

ISSN： 0385-2385
糖尿病性腎症におけるプロテアーゼ活性化受容体2(PAR2)の役割

大江佑治, 佐藤恵美子, 佐藤博, 伊藤貞嘉, 高橋信行

日本腎臓学会誌　57　(3)　502　2015/04/30

ISSN： 0385-2385
腹膜透析におけるグアニジノ化合物の動態と意義

佐藤恵美子, 森建文, 三枝大輔, 菅原真恵, 大場郁子, 小泉賢治, 千田真貴子, 永沼絵理, 佐藤博, 伊藤貞嘉

日本腎臓学会誌　57　(3)　565-565　2015/04/30
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
腹膜透析における(プロ)レニン受容体の動態と意義

矢花郁子, 森建文, 高橋知香, 佐藤恵美子, 大崎雄介, 鳴海かほり, 伊藤貞嘉

日本腎臓学会誌　57　(3)　462-462　2015/04/30
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
腹膜透析におけるインドキシル硫酸の動態と意義

佐藤恵美子, 森建文, 菅原真恵, 大場郁子, 三枝大輔, 小泉賢治, 千田真貴子, 永沼絵理, 佐藤博, 伊藤貞嘉

日本臨床分子医学会学術総会プログラム・抄録集　52回　85-85　2015/04
Publisher: 日本臨床分子医学会
2型糖尿病肥満モデルラットにおける長期的運動の腎一酸化窒素合成酵素および脂質酸化への影響

伊藤大亮, 曹鵬宇, 柿花隆昭, 須田千尋, 佐藤恵美子, 坂田佳子, 伊藤修, 上月正博, 清元秀泰

腎と脂質研究会プログラム・抄録集　27th　55　2015
腹膜透析患者における家庭血圧と生体インピーダンス法による体組成パラメーターの関連

倉澤奈穂, 森建文, 永沼絵理, 佐藤恵美子, 大場郁子, 小泉賢治, 佐藤真一, 土川未歩子, 伊藤貞嘉

日本腎臓リハビリテーション学会学術集会プログラム・抄録集　5th　185　2015
ニコチンアミドはAsb4欠損マウスの妊娠高血圧腎症,妊娠の維持,およびに胎児生存率を改善する

高橋信行, 高橋信行, 高橋信行, 伏間智史, LI Feng, 大江佑治, 佐藤恵美子, 佐藤恵美子, 佐藤博, 佐藤博, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　38th　405　2015
新規高感度ヘムオキシゲナーゼ活性測定法の開発

岩森紗希, 佐藤恵美子, 吉成浩一, 島田美樹, 眞野成康, 伊藤貞嘉, 佐藤博, 高橋信行

日本高血圧学会総会プログラム・抄録集　37回　332-332　2014/10
Publisher: (NPO)日本高血圧学会
腹膜透析におけるインドキシル硫酸クリアランスに及ぼす因子の検討

佐藤恵美子, 森建文, 菅原真恵, 大場郁子, 小泉賢治, 千田真貴子, 永沼絵理, 佐藤博, 伊藤貞嘉

JSBMS Lett　39　(Supplement)　100　2014/09/01

ISSN： 1881-5464
新規高感度ヘムオキシゲナーゼ活性測定法の開発

岩森紗希, 佐藤恵美子, 吉成浩一, 島田美樹, 眞野成康, 伊藤貞嘉, 佐藤博, 高橋信行

JSBMS Lett　39　(Supplement)　98-98　2014/09/01
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
腹膜透析におけるインドキシル硫酸クリアランスに及ぼす因子の検討

佐藤恵美子, 森建文, 菅原真恵, 大場郁子, 小泉賢治, 千田真貴子, 永沼絵理, 佐藤博, 伊藤貞嘉

JSBMS Letters　39　(Suppl.)　100-100　2014/09
Publisher: (一社)日本医用マススペクトル学会
ISSN： 1881-5464
慢性腎臓病における脳腎連関のメカニズム

森建文, 大崎雄介, 佐藤恵美子, 伊藤貞嘉

日本透析医学会雑誌　47　(Supplement 1)　378-378　2014/05/28
Publisher: (一社)日本透析医学会
ISSN： 1340-3451

eISSN： 1883-082X
新規高感度ヘムオキシゲナーゼ活性測定法の開発

岩森紗希, 佐藤恵美子, 吉成浩一, 島田美樹, 眞野成康, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　56　(3)　283-283　2014/05/25
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
ニコチン酸アミドのIgA腎症に対する治療効果

伏間智史, 大江佑治, 岩森紗希, 佐藤恵美子, 鈴木裕介, 富野康日己, 伊藤貞嘉, 佐藤博, 高橋信行

日本腎臓学会誌　56　(3)　388　2014/05/25

ISSN： 0385-2385
慢性腎臓病におけるアンジオテンシン代謝物のLC-MS/MSによる一斉分析

佐藤恵美子, 森建文, 鈴木深作, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本内分泌学会雑誌　89　(2)　741-741　2013/09
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
腹膜透析排液における(プロ)レニン受容体の検討

大場郁子, 森建文, 大崎雄介, 鳴海かほり, 佐藤恵美子, 小泉賢治, 丹野瑞穂, 島貫美和子, 千田真貴子, 堀内孝, 伊藤貞嘉

日本透析医学会雑誌　46　(Supplement 1)　501-501　2013/05/28
Publisher: (一社)日本透析医学会
DOI： 10.4009/jsdt.46.501 　

ISSN： 1340-3451

eISSN： 1883-082X
腹膜透析における上皮間葉形質転換を介した腹膜傷害機序の解明

大場郁子, 森建文, 大崎雄介, 佐藤恵美子, 中道淑美, 赤尾研人, 宮田敏男, 伊藤貞嘉

日本腎臓学会誌　55　(3)　326-326　2013/04/25
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
ヒトリンパ球および単球に存在する(プロ)レニン受容体の機能について

鳴海かほり, 廣瀬卓男, 佐藤恵美子, 森建文, 石井智徳, 伊藤貞嘉

日本内分泌学会雑誌　89　(1)　313　2013/04/01

ISSN： 0029-0661
地域健康診断における尿中アンジオテンシノージェンと血圧の関連~Kawasaki Study~

佐藤恵美子, 森建文, 中道淑美, 大場郁子, 吉田舞, 中道崇, 佐藤博, 伊藤貞嘉

日本内分泌学会雑誌　89　(1)　234-234　2013/04/01
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
地域健康診断における尿中アンジオテンシノージェンと血圧の関連 Kawasaki Study

佐藤恵美子, 森建文, 中道淑美, 大場郁子, 吉田舞, 中道崇, 佐藤博, 伊藤貞嘉

日本内分泌学会雑誌　89　(1)　234-234　2013/04
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
バイタルサイン実習:高機能患者シミュレータを用いた疾患模擬処置を「見学型」から「実践型」に切り替えたことによる学生の学習意欲調査

橋本貴尚, 高橋信行, 佐藤恵美子, 村井ユリ子, 平澤典保, 富岡佳久, 栃窪克行, 佐藤博

日本医療薬学会年会講演要旨集　22nd　484-484　2012/10/10
Publisher: 日本医療薬学会
炎症とRASのかかわりを探る慢性腎臓病と炎症とRAS

佐藤恵美子, 森建文, 伊藤貞嘉

Angiotensin Research　9　(4)　199-203　2012/10/01

ISSN： 1348-8740
【炎症とRASのかかわりを探る】慢性腎臓病と炎症とRAS

佐藤恵美子, 森建文, 伊藤貞嘉

Angiotensin Research　9　(4)　199-203　2012/10
Publisher: (株)先端医学社
ISSN： 1348-8740
若年層の生活習慣病予備群では腎内レニン・アンジオテンシシ系,酸化ストレスおよび炎症が亢進しているのか?

佐藤恵美子, 森建文, 中道淑美, 大場郁子, 佐藤博, 飛田渉, 伊藤貞嘉

日本内分泌学会雑誌　88　(2)　818　2012/09/20

ISSN： 0029-0661
若年層の生活習慣病予備群では腎内レニン・アンジオテンシン系、酸化ストレスおよび炎症が亢進しているのか?

佐藤恵美子, 森建文, 中道淑美, 大場郁子, 佐藤博, 飛田渉, 伊藤貞嘉

日本内分泌学会雑誌　88　(2)　818-818　2012/09
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661
透析患者痙攣症状に対するビオチン投与と血中ビオチン値測定

藤原正子, 小熊司郎, 安藤一郎, 佐藤恵美子, 佐藤博, 今井潤, 関野宏

日本透析医学会雑誌　45　(Supplement 1)　487　2012/05/28

ISSN： 1340-3451
メチルグリオキサールによる腹膜傷害に対するGLO‐1の役割

大場郁子, 森建文, 佐藤恵美子, 米城淑美, 赤尾研人, 宮田敏男, 伊藤貞嘉

日本腎臓学会誌　54　(3)　221　2012/04/25

ISSN： 0385-2385
ヒトリンパ球における(プロ)レニン受容体の検討

鳴海かほり, 森建文, 石川繭子, 佐藤恵美子, 廣瀬卓男, 石井智徳, 伊藤貞嘉

日本腎臓学会誌　54　(3)　257　2012/04/25

ISSN： 0385-2385
アンジオテンシン代謝産物のLC‐MS/MSによる測定

佐藤恵美子, 森建文, 大場郁子, 鈴木深作, 芦毅, 石川繭子, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本腎臓学会誌　54　(3)　302-302　2012/04/25
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
腎髄質循環におけるミトコンドリアストレス

森建文, 芦毅, 赤尾研人, 大場郁子, 佐藤恵美子, 伊藤貞嘉

日本腎臓学会誌　54　(3)　196　2012/04/25

ISSN： 0385-2385
LC/MS/MSによる生体内アンジオテンシン代謝物の測定法の開発

佐藤恵美子, 森建文, 鈴木深作, 芦毅, 石川繭子, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本内分泌学会雑誌　88　(1)　340-340　2012/04/01
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
アンジオテンシン代謝産物のLC-MS/MSによる測定

佐藤恵美子, 森建文, 大場郁子, 鈴木深作, 芦毅, 石川繭子, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本腎臓学会誌　54　(3)　302-302　2012/04
Publisher: (一社)日本腎臓学会
ISSN： 0385-2385

eISSN： 1884-0728
若年肥満者の高血圧と尿中バイオマーカーの関連

佐藤恵美子, 森建文, 米城淑美, 大場郁子, 伊藤貞嘉

日本高血圧学会臨床高血圧フォーラムプログラム・抄録集　1回　137-137　2012/04
Publisher: (NPO)日本高血圧学会
LC/MS/MSを用いた生体試料中スフィンゴ脂質同時定量法の構築

芝可奈子, 三枝大輔, 井上飛鳥, 濱弘太郎, 奥谷倫世, 鈴木千登世, 佐藤恵美子, 眞野成康, 菱沼隆則, 鈴木直人, 佐藤博, 阿部高明, 青木淳賢, 富岡佳久

日本薬学会年会要旨集　132nd　(4)　138-138　2012/03/05
Publisher: (公社)日本薬学会
ISSN： 0918-9823
【生活習慣病とミトコンドリア異常】慢性腎臓病(CKD)発症とミトコンドリア酸化ストレス

佐藤恵美子, 森建文, 伊藤貞嘉

Medical Science Digest　38　(2)　65-68　2012/02
Publisher: (株)ニュー・サイエンス社
ISSN： 1347-4340
Establishment of a new measurement method of angiotensin using a LC/MSMS

大場郁子, 佐藤恵美子, 森建文, 鈴木深作, 芦毅, 石川繭子, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本抗加齢医学会総会プログラム・抄録集　12th　197-197　2012
Publisher: (一社)日本抗加齢医学会
若年肥満者における尿中カルボニル物質による血圧上昇の予測

佐藤恵美子, 森建文, 川俣彰裕, 米城淑美, 飛田渉, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　34th　523　2011/10/20
リアルタイムイメージングによる腎尿細管上皮細胞のブドウ糖誘導性ミトコンドリア内酸化ストレスの検討

芦毅, 森建文, 佐藤恵美子, 清元秀泰, 小川晋, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　34th　588　2011/10/20
若年肥満者における尿中カルボニル物質による血圧上昇の予測

佐藤恵美子, 森建文, 川俣彰裕, 米城淑美, 飛田渉, 伊藤貞嘉

日本高血圧学会総会プログラム・抄録集　34回　523-523　2011/10
Publisher: (NPO)日本高血圧学会
LC/MS/MSによる生体内アンジオテンシン代謝産物の測定法の確立

大場郁子, 佐藤恵美子, 森建文, 鈴木深作, 芦毅, 石川繭子, 後藤貴章, 佐藤博, 大江知行, 伊藤貞嘉

日本内分泌学会雑誌　87　(2)　779　2011/09/20

ISSN： 0029-0661
ヒトリンパ球に存在する(プロ)レニン受容体の発現検討

鳴海かほり, 森建文, 石川繭子, 佐藤恵美子, 石井智徳, 廣瀬卓男, 伊藤貞嘉

日本内分泌学会雑誌　87　(2)　784　2011/09/20

ISSN： 0029-0661
In vitro再構成NADH oxidase系およびxanthine oxidase系における活性酸素種の動態解析

庭野吉己, 佐藤恵美子, 目代貴之, 河野雅弘

日本酸化ストレス学会学術集会プログラム・抄録集　64th　2011
LC‐MSを用いた慢性腎臓病患者血漿の腎障害マーカーの研究(II)

相澤純子, 佐藤恵美子, 河野雅弘, 藤澤達也, 藤原功一, 田仲紀陽

JSBMS Letters　35　(Supplement)　66　2010/08/03

ISSN： 1881-5464
LC‐MSを用いた透析患者血漿中のメタボローム解析(III)

佐藤恵美子, 相澤純子, 河野雅弘, 藤澤達也, 藤原功一, 田仲紀陽

JSBMS Lett　35　(Supplement)　65　2010/08/03

ISSN： 1881-5464
In vitroスーパーオキサイド発生酵素:キサンチンオキシダーゼ・NAD(P)Hオキシダーゼの評価

佐藤恵美子, 八重柏典子, 庭野吉己, 河野雅弘

日本酸化ストレス学会学術集会プログラム・抄録集　63rd　138　2010/06/24
ESRスピントラップ法を用いたラジカル定量の潜在的問題

佐藤恵美子, 中村圭祐, 菅野太郎, 猪飼紘代, 目代貴之, 庭野吉己, 小澤俊彦, 河野雅弘

日本酸化ストレス学会学術集会プログラム・抄録集　63rd　128　2010/06/24
LC‐MSを用いた慢性腎臓病患者血漿の腎障害マーカーの研究

佐藤恵美子, 相澤純子, 河野雅弘, 藤沢達也, 藤原功一, 田仲紀陽

質量分析総合討論会講演要旨集　58th　195　2010/06/01
活性酸素生成酵素キサンチンオキシダーゼ,NADHオキシダーゼ反応における新規活性中間体HOOOHの形成機構

佐藤恵美子, 庭野吉己, 八重柏典子, 目代貴之, 河野雅弘

日本酸化ストレス学会学術集会プログラム・抄録集　62nd　69　2009/06/11
化学発光における末梢血好中球と口腔内好中球の細胞応答の違い

八重柏典子, 佐藤恵美子, 中村圭祐, 猪飼紘代, 林栄成, 菅野太郎, 河野雅弘

日本酸化ストレス学会学術集会プログラム・抄録集　62nd　117　2009/06/11
Existence of a new reactive intermediate oxygen species in hypoxanthine and xanthine oxidase reaction (vol 56, pg 1194, 2008)

E. Sato, T. Mokudai, Y. Niwano, M. Kamibayashi, M. Kohno

CHEMICAL & PHARMACEUTICAL BULLETIN　57　(6)　646-646　2009/06

ISSN： 0009-2363
LC‐MSを用いた透析患者血漿中のメタボローム解析(1)

佐藤恵美子, 河野雅弘, 山本昌則, 藤沢達也, 藤原功一, 田仲紀陽

質量分析総合討論会講演要旨集　57th　570-571　2009
アグリバイオ実用化・産業化研究第6章ラフィド藻・渦鞭毛藻等赤潮の原因となるプランクトンが産生する新規生理活性物質の機能解明及び大量生産技術の開発

松山幸彦, 庭野吉己, 倉智麻木, 内山元子, 別府史章, 板倉茂, 赤根幸子, 影山裕子, 小田達也, 中島琢自, 金大景, 宮崎洋介, 河野雅弘, 佐藤恵美子, 目代貴之

農林水産省農林水産技術会議事務局研究成果　(458)　2008
ケミルミネッセンス化学発光法の最近の進歩

佐藤恵美子, 河野雅弘

マテリアルライフ学会誌　19　(4)　155-162　2007/10/31
Publisher: MATERIALS LIFE SOCIETY, JAPAN
DOI： 10.11338/mls2001.19.155 　

ISSN： 1346-0633
LC‐TOF‐MSを用いた花粉症患者の血漿分析

田中章子, 高橋美穂, 佐藤恵美子, 柴田浩樹, 石川多恵子, 河野雅弘

アレルギー　56　(8/9)　1125-1125　2007/09/30
Publisher: 一般社団法人日本アレルギー学会
DOI： 10.15036/arerugi.56.1125_2 　

ISSN： 0021-4884
赤潮プランクトン水抽出物中のO₂^- 消去物質

佐藤恵美子, 鹿野吉己, 鹿野吉己, 河野雅弘, 倉智麻木, 松山幸彦, 金大景, 山口健一, 小田達也

日本水産学会大会講演要旨集　2007　12　2007/09/25
赤潮プランクトン水抽出物の抗酸化特性

庭野吉己, 佐藤恵美子, 河野雅弘, 松山幸彦, 金大景, 小田達也

日本水産学会大会講演要旨集　2007　11　2007/09/25
LC‐TOFMSによる花粉症患者の血漿分析―メタボロミクスアプローチによる解析

高橋美穂, 佐藤恵美子, 田中章子, 石川多恵子, 柴田浩樹, 河野雅弘

質量分析総合討論会講演要旨集　55th　376-377　2007/05/01
LC/MSによる血漿中ジカルボニル物質3種の同時測定

中山恵輔, 佐藤恵美子, 高橋美穂, 寺脇博之, 中山昌明, 伊藤貞嘉, 河野雅弘

質量分析総合討論会講演要旨集　55th　404-405　2007/05/01
渦鞭毛藻類赤潮プランクトン抽出物のスーパーオキシド消去活性―化学発光法とESR‐スピントラッピング法での乖離―

佐藤恵美子, 庭野吉己, 目代貴之, 河野雅弘, 松山幸彦, 金大景, 小田達也

日本水産学会大会講演要旨集　2007　113　2007/03/28
渦鞭毛藻類赤潮プランクトンはスーパーオキシド消去物質を産生する

庭野吉己, 佐藤恵美子, 河野雅弘, 松山幸彦, 金大景, 中島琢自, 小田達也

日本水産学会大会講演要旨集　2007　113　2007/03/28
RAW264.7細胞のNADPHオキシダーゼに対するプロジギオシン誘導体の影響

中島琢自, 佐藤恵美子, 倉智麻木, 山口健一, 庭野吉己, 小田達也

日本農芸化学会大会講演要旨集　2006　2006

Show all ︎Show first 5

Industrial Property Rights 7

慢性腎臓病の病期を判定する方法又は装置若しくはその作動方法

田仲紀陽, 河野雅弘, 佐藤恵美子, 藤原功一

Property Type: Patent
腎疾患重篤度を判定する方法又は装置若しくはその作動方法

田仲紀陽, 河野雅弘, 佐藤恵美子, 藤原功一

Property Type: Patent
癌罹病の検定に使用するデータの収集方法

河野雅弘, 大内憲明, 武田元博, 佐藤恵美子, 高橋美穂, 山田理恵

Property Type: Patent
ヒドロキシルラジカル消去剤、ならびにこれを含む食品、薬品および化粧料

庭野吉己, 佐藤恵美子, 松山幸彦, 小田達也, 金大景

Property Type: Patent
抗酸化剤、ならびにこれを含む食品、薬品および化粧料

庭野吉己, 佐藤恵美子, 松山幸彦, 小田達也, 金大景

Property Type: Patent
慢性腎臓病の病期を判定する方法又は装置若しくはその作動方法

田仲紀陽, 河野雅弘, 佐藤恵美子, 藤原功一

特許第5832429号

Property Type: Patent
腎疾患重篤度を判定する方法又は装置若しくはその作動方法

田仲紀陽, 河野雅弘, 佐藤恵美子, 藤原功一

特許第5197846号

Property Type: Patent

Show all Show first 5

Research Projects 23

ヒストン脱メチル化酵素欠損と胎生致死および新規妊娠高血圧腎症モデルの開発

高橋信行, 佐藤恵美子, 山越聖子

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 基盤研究(C)

Institution: 東北大学

2024/04/01 - 2029/03/31
尿毒素による細胞内代謝失調を標的とした高齢者の慢性腎臓病合併症の治療開発

佐藤恵美子, 吉田舞, 山越聖子, 宮崎真理子, 元池育子, 田中哲洋, 三枝大輔

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 基盤研究(B)

Institution: 東北大学

2024/04/01 - 2027/03/31
尿毒素による細胞内代謝失調を標的とした高齢者の慢性腎臓病合併症の治療開発

佐藤恵美子

Offer Organization: 日本学術振興会

System: 科学研究費助成事業基盤研究(B)

Category: 基盤研究(B)

Institution: 東北大学

2023/04/01 - 2027/03/31
早産・低出生体重児の将来の腎臓病リスクを軽減する超先制治療の開発

佐藤恵美子, 山越聖子

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 挑戦的研究(萌芽)

Institution: 東北大学

2024/06/28 - 2026/03/31
Is the prevention of low birth weight infants by maternal treatment effective in preventing the onset of adult diseases in infants?

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2022/04/01 - 2025/03/31
CKD患者のサルコペニアの病態機序解明およびHIF-PH阻害薬の効果に関する検討

渡邉公雄, 佐藤恵美子, 中山昌明

Offer Organization: 日本学術振興会

System: 科学研究費助成事業基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2022/04/01 - 2025/03/31
ニコチンアミドによる慢性腎臓病の治療・予防と新規治療薬の開発

高橋信行, 佐藤恵美子, 堰本晃代

Offer Organization: 日本学術振興会

System: 科学研究費助成事業基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2021/04/01 - 2024/03/31

More details Close

腎臓で血液をろ過する糸球体の障害をきっかけとして、徐々に腎臓全体が障害されて腎不全になるタイプの慢性腎臓病は多い。しかし、その病態には不明な点が多く、治療法も確立していない。最近、研究代表者らは腎臓で体液の水分塩分などの量の調節を行う尿細管という部分の障害による慢性腎臓病をビタミンB3であるナイアシン（ニコチンアミド）がATP産生を増加することなどによって予防することを明らかにした。抗ガン剤のアドリアマイシンによっておこる動物モデルは糸球体障害による慢性腎臓病の研究によく用いられている。本研究ではアドリアマイシンによっておこる糸球体障害がニコチンアミドで予防や治療ができるか明らかにすることを目的とした。当該年度の研究において、マウスにアドリアマイシンを投与すると、ネフローゼ症候群に匹敵する大量の蛋白（アルブミン）の尿中への排泄が認められた。次に、糸球体障害による慢性腎臓病で患者数も多いIgA腎症に注目した。IgA腎症は腎不全へ進行し、透析などが必要になることが少なくない。さらに、IgA腎症は妊娠可能年齢の女性にも多い。本研究において、IgA腎症に対するニコチンアミドの効果を明らかにすることを目的として、IgA腎症のマウスモデルであるgddYマウスを用いた。gddYマウスのオスへのニコチンアミド投与は、腎機能、腎病理所見を改善しなかったが、生存率、炎症性サイトカインや線維化に関連する遺伝子の腎臓での発現を低下させた。また、メスgddYマウスの正常妊娠および妊娠高血圧症候群（妊娠中毒症）のモデルを作成した。ニコチンアミドは、妊娠高血圧症候群とIgA腎症の進行を抑制する傾向をもたらした。
Elucidating the pathogenic mechanism of CKD-associated cognitive dysfunction and muscle wasting as revealed by metabolic changes in organs

Sato Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2019/04/01 - 2022/03/31

More details Close

Chronic kidney disease (CKD)-associated cognitive dysfunction and muscle wasting are important problems with the aging of the patients with CKD. In this study, we elucidated the pathogenesis of CKD-associated cognitive dysfunction and muscle wasting using cell line and animal disease model. We first evaluated the effects of various uremic toxins on the mouse myoblast cell line C2C12 and the mouse hippocampal neuronal cell line HT-22. We found that indoxyl sulfate and indole negatively affected the hippocampal neuronal cell line, and that methylglyoxal induced intracellular metabolic changes and decreased ATP production in only myoblasts. Furthermore, we found that intracellular metabolic changes are also induced in the kidney in CKD model mouse, and that nicotinamide treatment protect the progression of the CKD dysfunction.
Studies of therapeutic medicines for pregnancy complicated with renal disease

Sato Hiroshi

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2017/04/01 - 2020/03/31

More details Close

In this study, we focused on pregnancy with systemic lupus erythematosus (SLE) and IgA nephropathy as pregnancies with renal disease. These diseases are prevalent among women in their 20s and 40s who can be pregnant. In addition, pregnancy with these diseases is frequently associated with miscarriage/premature birth, fetal growth restriction, preeclampsia-like symptoms, etc., and pregnancy prognosis is poor. Therefore, it is an urgent need to develop new therapeutic medicines. We have already shown that nicotinamide, which is a vitamin B3, is a medicine that can be administrated to pregnant women and improves oxidative stress and endothelial dysfunction in preeclampsia model mice. In this study, we also found that nicotinamide showed therapeutic effects such as suppression of hypertension and improvement of fetal growth restriction in pregnancies with SLE or IgA.
Physiological and molecular mechanisms underlying renal congestion in congestive heart failure

MORI Takefumi, SHIMADA Satoshi, TAKAHASHI Chika

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku Medical and Pharmaceutical University

2016/04/01 - 2019/03/31

More details Close

We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. Tubulointerstitial injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Using this rat congestion model and cell culture system, we revealed that vacuolar ATPase system in acidic organelles and pericyte injury were involved in the development of renal interstitial fibrosis due to renal congestion.
Uremic sarcopenia induced by uremic toxins in chronic kidney disease

Sato Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2016/04/01 - 2019/03/31

More details Close

Sarcopenia is associated with increased morbidity and mortality in chronic kidney disease (CKD). Pathogenic mechanisms of skeletal muscle loss in CKD remains unclear. Renal dysfunction results in the accumulation of various uremic toxins in the circulation. The accumulation of uremic toxins has been proposed as a contributing factor for sarcopenia in CKD. In this study, we examined the association between uremic toxins and sarcopenia using myoblast cell line C2C12, adenine-induced renal failure model mouse, and CKD patients. From our results, it indicated that uremic toxin indoxyl sulfate is a pathogenic factor for sarcopenia in CKD. Futhermore, we revealed that causative pathological mechanism of uremic sarcopenia is metabolic alteration causes ATP shortage in muscle cells.
抗HIV/HBV薬テノホビルジソプロキシルフマル酸塩関連腎障害の病態解明および予防法の検討 Competitive

佐藤恵美子

Offer Organization: 公益財団法人鈴木謙三記念医科学応用研究財団

2017 - 2018
糖尿病性腎症の発症機序に基づいた早期診断および薬効マーカーの探索と治療におけるエピジェネティックな遺伝子発現調節機構の変化 Competitive

佐藤恵美子

Offer Organization: 公益財団法人内藤記念科学振興財団

System: 女性研究者研究助成金

2016 - 2018
イメージングMS可視化によるウレミックサルコペニアの機構解明と治療薬の探 Competitive

佐藤恵美子

Offer Organization: 日本学術振興会

System: 科研費基盤研究C

2016 - 2018
Evaluation of the function of (pro)renin receptor in chronic kidney disease and autoimmune disease

Narumi Kaori, Sato Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity Start-up

Category: Grant-in-Aid for Research Activity Start-up

Institution: Tohoku University

2015/08/28 - 2017/03/31

More details Close

We collected sera from patients diagnosed with immunoglobulin A nephropathy by renal biopsy and examined the correlation between serum soluble (P)RR [s(P)RR] and various laboratory data and pathological indices. The s(P)RR level significantly correlated with the level of mesangial expansion and serum indoxyl sulfate (IS). To investigate the association between (P)RR and mesangial fibrosis or expansion, we used mouse mesangial cell line SV40 MES13. (P)RR expression significantly increased in the presence of IS. IS stimulation enhanced the expression of the fibrotic factors, this increased expression was significantly suppressed by knockdown of (P)RR. Moreover, it significantly increased the expression of tissue inhibitor of metalloproteinase type 1 and matrix metalloproteinase 9 via the ERK1/2 pathway in SV40 MES13 cells. Our results suggest that in the presence of IS, (P)RR is associated with mesangial fibrosis and matrix expansion through the (P)RR-mediated ERK1/2 pathway.
A new therapy for blood purification of oxidative stress and uremic toxin verified by mouse kidney transplantation

Abe Michiaki, OKUDA HIROSHI

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2013/04/01 - 2016/03/31

More details Close

The project including a mouse kidney transplantation was extremely so difficult to accomplish in Japan that our graduate student studied abroad and carry forward the experiment in Duke University Medical Center, kidney research institute (Prof. Coffman TM) one and a half years ago. The donor mouse kidney, the size as same as adzuki bean, is quickly transplanted to a recipient mouse under an ophthalmologic microscope in 11-0 suture without injuring the renal artery, vein and ureter. This project has been going still now. The final aim of this project is development of a new therapeutic agent for chronic kidney disease by blood purification of uremic material and oxidation stress. As the new candidate drug was found, I started a cohort study of it.
Exploration of specific biomarkers for carbonyl stress inducible disease.

ITO Sadayoshi, MORI Takefumi, NIWANO Yoshimi, SATO Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2012/04/01 - 2015/03/31

More details Close

Administration of methylglyoxal (MG) to Dahl salt sensitive rats increased blood pressure, renal injury and cardiac-fibrosis. Simultaneously treatment with angiotensin II (AngII) receptor blocker (ARB) ameliorated MG induced blood pressure increase, renal injury and cardiac injury. These results indicate that renin angiotensin system (RAS) partially contribute hypertension and organ injury induced by carbonyl stress. Since RAS is involved in inflammation, we evaluated the contribution of (pro)renin receptor [(P)RR] to inflammatory reaction. Renin stimulation induced ERK phosphorylation, COX-2 mRNA expression and IL-6 secretion in human peripheral blood mononuclear cells. (P)RR siRNA treatment ameliorated ERK phosphorylation induced by renin stimulation in human leukemic monocyte lymphoma cells. These results indicates that (P)RR could contribute inflammatory response in human inflammatory cells.
Development and application of order-made dignosis using omics-integrated analysis of chronic kidney disease and hemodialysis patients

TAKEUCHI KAZUHISA, FUJIWARA Masako, TOTSUNE Kazuhito, SATO Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2012/04/01 - 2015/03/31

More details Close

For development of order-made diagnostis for chronic kidney disease and hemodailysis (HD) patients, we applied omocs-integrated analysis of plasma and dialysate from HD patients. To investigate metabolic responses to HD, we have determined levels of metabolites by nuclear magnetic resonance (1H NMR) spectroscopy of dialysate during HD. Unlike the response of creatinine, lactate, pyruvate and alanine exhibited increments at the middle time of HD. The time-course of changes in these metabolites was unique to each patient. Muscle cramp is a common complications of HD. We defined score of the cramps and measured the effects of oral administration of biotin to cramps. We measured plasma biotin levels of the patients before prescribed biotin by ELISA methods, and found they were dependent on the efficacies of prescribed biotin. The fact of fenome (cramp scores) and metabolome (biotin levels) were correlated may provide information to the order-made diagnosis of HD patients.
Exploration of less-invasive biomarkers for chronic kidney disease

SATO Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)

Category: Grant-in-Aid for Young Scientists (B)

Institution: Tohoku University

2012/04/01 - 2015/03/31

More details Close

Residual renal function is an important predictor of 1-year mortality in chronic kidney dialysis patients. In this study, we explored the biomarker of residual renal function (RRF) in peritoneal dialysis patients (PD). Sixteen PD patients (64 ± 11 years, men:10, women;6) were intended to this study. Blood and PD fluids sample were collected in peritoneal equilibration test (PET). Seventeen uremic toxins were quantified by LC-MS/MS. Relationship between plasma uremic toxin concentration and clinical parameters, RRF and InBody data was evaluated. From the results, plasma indoxyl sulfate (IS) and methylguanidine (MG) increased in PD patients in parallel with loss of RRF, but not peritoneal function. Furthermore, plasma concentrations of IS and MG were significantly correlate with body muscle mass. Our data suggested that plasma concentrations of IS and MG were increased with loss of RRF and they affect body muscle.
慢性腎臓病患者予備軍への低侵襲早期診断マーカーの探索と検討 Competitive

佐藤恵美子

Offer Organization: 日本学術振興会

System: 科研費若手研究B

2012 - 2015
Role of ADP ribosyl cyclase in pathogenesis of preeclampsia

TAKAHASHI NOBUYUKI, SATO Hiroshi, SATO Emiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

Category: Grant-in-Aid for Challenging Exploratory Research

Institution: Tohoku University

2012/04/01 - 2014/03/31

More details Close

Pre-eclampsia (PE), hypertension and proteinuria developing after 20 weeks of gestation, is the cause of maternal and fetal deaths. The only definitive treatment currently available to save the mother and/or the baby is induced delivery. Anti-hypertensives acceptable for use during pregnancy help control maternal blood pressure in PE, but they do not prevent pre-term delivery nor correct the fetal growth restriction associated with PE. We have demonstrated that nicotinamide reduces the hypertension and proteinuria in mice having a pre-eclampsia-like condition, delays miscarriages and alleviates the fetal growth restriction. Nicotinamide is the first substance that benefits both mother and offspring by targeting a pathway specifically dysfunctional in PE. It merits evaluation for preventing or treating PE in humans.
慢性腎臓病患者予備軍への低侵襲早期診断マーカーの探索 Competitive

佐藤恵美子

Offer Organization: 日本学術振興会

System: 科研費若手研究B

2011 - 2012
慢性腎臓病患者予備軍への低侵襲早期診断マーカーの探索

佐藤恵美子

Offer Organization: 日本学術振興会

System: 科学研究費助成事業若手研究(B)

Category: 若手研究(B)

Institution: 東北大学

2011 - 2011

More details Close

本研究では、早期に腎障害を発見するためのバイオマーカーを探索することを目的としていた。申請者のこれまでの研究で、透析患者の血漿成分を透析前後で比較を行い、マーカー候補を複数見出していた。本研究では、(1)診断のためのマーカーに関する研究、(2)診断のための感度と特異度を向上するマーカーの選別、(3)診断マーカーの構造解明を行うことで、早期腎障害診断マーカーを発見することを目指した。23年度はマーカー候補成分のCKD患者の病期ステージごとの動態についての研究と診断のための感度と特異度を向上するマーカーの選別研究を計画していた。しかし、震災の影響で使用予定であった質量分析装置は破壊されたため、使用できなくなった。そのため使用可能な共通機器である質量分析装置を使用することになったが、使用申請やトレーニング等により当初の研究予定は大幅に遅れをとった。そこで平成23年度は慢性腎臓病(CKD)患者の血漿と尿試料の回収と、前処理条件と測定条件の検討を行った。検体を回収した患者は、CKDであり腹膜透析治療を受けている患者であるため、測定試料として透析治療前と透析治療後の血漿と尿、さらに腹膜透析廃液を回収している。得られた血漿、尿、透析廃液を用いて、前処理法と測定条件の検討を行った。その結果、前処理・測定条件の確立には、まだ検証することが残っているが、血漿、尿、腹膜透析液から目的とする腎臓病に関与する成分をクリーンアップすることが可能であることが分かった。本研究が目的とする成分は、これまで単一成分を放射性免疫測定や酵素法免疫測定で測定されていたが、本研究の方法で多成分を同一試料から測定できることが分かった。この方法を用いることで、腎臓代謝の状況を判断することができ、腎障害を早期に発見できる可能性が示された。

Show all Show first 5

Teaching Experience 5

学問論演習
臨床薬理学
薬物療法学３
機能形態学２
医療薬学基礎実習