| Project/Area Number |
21590938
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
MATOBA Satoaki 京都府立医科大学, 医学研究科, 助教 (10305576)
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| Co-Investigator(Kenkyū-buntansha) |
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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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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 | p53 / 心不全 / ミトコンドリア / エネルギー代謝 / アポトーシス |
|---|
| Research Abstract |
Ischemia or hyperglycemia induced p53, SCO2(Synthesis of cytochrome c oxidase 2) and TIGAR(TP53-induced glycolysis and apoptosis regulator) in the heart. We demonstrated diabetic condition induced SCO2, which promoted cardiac lipotoxicity(Circ Heart Fail. 2012). Ischemia induced p53 and TIGAR, which inhibited glycolysis(Am J Physiol Heart Circ Physiol. 2010) and mitophagy in the myocardium(J Mol Cell Cardiol. 2012). We also found that p53/TIGAR-mediated inhibition of myocyte mitophagy was responsible for ventricular remodeling after myocardial infarction.(J Mol Cell Cardiol 2012). SCO2 heterozygote mice were protective against diabetes induced cardiomyopathy. These data indicated that regulating energy metabolism will be a novel therapeutics for heart failure.
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