| Project/Area Number |
25460316
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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 |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Kohsaka Akira 和歌山県立医科大学, 医学部, 准教授 (00458051)
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| Co-Investigator(Kenkyū-buntansha) |
Waki Hidefumi 順天堂大学, スポーツ健康科学部, 准教授 (50274957)
Gouraud Sabine お茶の水女子大学, 理学部, 研究員 (30453179)
Otsuka Tsuyoshi 和歌山県立医科大学, 医学部, 学内助教 (60760395)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | 心不全 / 時計遺伝子 / ミトコンドリア |
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| Outline of Final Research Achievements |
Dysfunction of the circadian system has been shown to induce a malfunction of many organs including the heart. However, little is known about how the circadian clock regulates heart function. In the present study, we found that a heart-specific knockout of Bmal1, a core circadian clock gene, leads to age-dependent cardiomyopathy in mice. DNA microarray analysis revealed that expression levels of genes controlling energy metabolism such as mitochondrial biogenesis and ATP production are altered in the heart tissue of knockout animals. In addition, both function and morphology of mitochondria in cardiomyocytes are disrupted in heart-specific Bmal1 knockout mice. Together, our results indicate that the circadian clock in the heart plays an important role in regulating mitochondrial energetics, and thereby maintains heart function in mammals.
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