| Project/Area Number |
21590939
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
|
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| Research Institution | Meiji University of Integrative Medicine (2010-2011)
Kyoto Prefectural University of Medicine (2009) |
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Principal Investigator |
IWAI-KANAI Eri 明治国際医療大学, 医学教育研究センター, 教授 (20372584)
|
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| Co-Investigator(Kenkyū-buntansha) |
MATOBA Satoaki 京都府立医科大学, 医学研究科, 助教 (10305576)
|
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
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| Keywords | 心不全 / ミトコンドリア / 細胞死 / オートファジー |
|---|
| Research Abstract |
Using a new method for cardiac autophagy which was established by us, we examined the mechanism of cardiac repair in the progress of heart failure. Cardiac autophagy was accelerated in the early phase of heart failure, which was key for cardiac protection. In the heart of metabolic disorder, ischemia, or anti-cancer drug, the control of cardiac autophagy was impaired and p53-TIGAR pathway acted as a critical role for cardiac cellular fate.
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