2011 Fiscal Year Final Research Report
Strategy for overcoming chronic kidney disease, focusing on mineralocorticoid receptor
| Project/Area Number |
21390261
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
NAGASE Miki 東京大学, 医学部附属病院, 特任准教授 (60302733)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITA Toshiro 東京大学, 医学部附属病院, 教授 (10114125)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 慢性腎臓病 / 生活習慣病 / 糸球体足細胞障害 / アルドステロン / Racl |
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| Research Abstract |
We previously reported that overactivation of the mineralocorticoid receptor(MR), a receptor for aldosterone, plays a crucial role in the progression of chronic kidney disease, and identified a novel mechanism of MR activation by the small G protein Rac1. In this study, we showed that´MR activation by Rac1' participates in the renal damage of angiotensin II and salt excess model, obese diabetes model, as well as in salt-sensitive hypertension. We also demonstrated that'Rac1-mediated MR activation' contributes to the inflammatory mechanism of kidney impairment.
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Research Products
(43 results)
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[Journal Article] Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptor-dependent pathway2011
Author(s)
Shibata S, Mu S, Kawarazaki H, Muraoka K, Ishizawa K, Yoshida S, Kawarazaki W, Takeuchi M, Ayuzawa N, Miyoshi J, Takai Y, Ishikawa A, Shimosawa T, Ando K, Nagase M, Fujita T.
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Journal Title
J Clin Invest
Volume: 121(8)
Pages: 3233-43
DOI
Peer Reviewed
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