| Project/Area Number |
26461236
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
脇野 修 慶應義塾大学, 医学部(信濃町), 准教授 (50265823)
林 晃一 東京歯科大学, 歯学部, 教授 (80164937)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | rho-kinase / mDia / p27 / proximal tubule / cell cycle / Rhoキナーゼ / RhoA / PHD2 / Rho / Cell Cycle / 虚血 / PHD / HIF / 肥満関連腎症 / 近位尿細管 |
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| Outline of Final Research Achievements |
Excess fat intake causes obesity-induced renal injury, which are mediated by an activated Rho/Rho-kinase pathway in proximal tubules and inflammatory process. It is surmised that hypertrophic process in proximal tubules during obesity formation affects Rho-kinase activation presumably through mechanical stress. mDia is induced in an early phase and subsequently the induction of Rho-kinase is observed in obesity. In parallel with that, p27 is suppressed, thereby leading to the hyperplastic state of cell cycle, which is contrary to the hypoplastic state in diabetes. This process subsequently induces inflammation and accelerates the histological changes of proximal tubules. The intervention of Rho/Rho-kinase may constitute a novel strategy blocking the progression process of obesity-induced renal damages from an early stage.
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