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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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2010: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2009: ¥8,580,000 (Direct Cost: ¥6,600,000、Indirect Cost: ¥1,980,000)
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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 / 糸球体足細胞 / Rac1 / 鉱質コルチコイド受容体 / メタボリックシンドローム / Sgk1 |
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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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Report
(4 results)
Research Products
(165 results)
