| Project/Area Number |
24791059
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Kyoto University |
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Principal Investigator |
BABA Shiro 京都大学, 医学(系)研究科(研究院), 助教 (60432382)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | デュシェンヌ型筋ジストロフィー / 心筋症 / iPS細胞 / カルシウム代謝 / Duchenne型筋ジストロフィー / 肥大型心筋症 / 心不全 |
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| Research Abstract |
Duchenne muscular dystrophy (DMD) frequently causes cardiomyopathy. Because of development of home respirator and oxygen treatment, a death rate by respiratory failure has been remarkably reduced and the patients live longer than before. In contrast, the death rate by heart failure is increasing. To reveal mechanisms of developing cardiomyopathy in DMD patients, we generated iPSC from a DMD patient and differentiated cardiomyocytes from the iPS cells. When we measured intracellular free calcium ion concentration, calcium level was remarkably elevated in the cardiomyocytes derived from DMD-iPS cardiomyocytes. Moreover, calcium overload was observed much more clearly in cardiomyocytes derived from DMD-iPSCs than in cardiomyocytes derived from control-hiPSCs after compulsory stretching.These findings indicated that calcium overload is one of the mechanisms for cardiomyopathy in DMD patients. Reducing calcium overload will be one of the treatments for DMD cardiomyopathy patients.
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