2010 Fiscal Year Final Research Report
Pathophysiological role of TRPV2 as a therapeutic target for cardiomyopathy/heart failure
| Project/Area Number |
20590874
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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 | National Cardiovascular Center Research Institute |
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Principal Investigator |
IWATA Yuko National Cardiovascular Center Research Institute, 分子生理部, 室長 (80171908)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 心筋症 / 心不全 / イオンチャネル / カルシウム |
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| Research Abstract |
We identified TRPV2 as a principal candidate for Ca^<2+>-entry pathways which result in abnormal Ca^<2+> handling in muscular degeneration caused by cytoskeleton abnormality. Inhibition of endogenous TRPV2 significantly reduced the increase in basal intracellular Ca^<2+> and stretch-induced damage as well as improved muscle function in animal models. These data suggest that enhanced TRPV2 activity is important to trigger muscle damage and that it is a promising therapeutic target for muscular dystrophy and cardiomyopathy.
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