2013 Fiscal Year Final Research Report
Improvement of therapeutic methods for cardiomyopathy/heart failure based on the functional analysis of stretch-activated ion channel
| Project/Area Number |
23591095
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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 |
Circulatory organs internal medicine
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
IWATA Yuko 独立行政法人国立循環器病研究センター, 研究所, 室長 (80171908)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 心筋症 |
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| Research Abstract |
Dilated cardiomyopathy (DCM) is a severe disorder defined by ventricular dilation and cardiac dysfunction. A subset of familial DCM is caused by mutations of the genes encoding cytoskeleton. Here, we show that transient receptor potential vanilloid 2 (TRPV2) is highly concentrated in the ventricular sarcolemma of patients with idiopathic DCM and animal models of cardiomyopathy. We found some tools to inhibit the surface expression of and Ca2+ influx via TRPV2. In the animal models, blockade of TRPV2 ameliorated cardiac dysfunction, and prevented DCM progression; Therefore, we propose that sarcolemmal accumulation or activation of TRPV2 initiated by membrane instability resulting from cytoskeleton abnormalities contributes to cardiac dysfunction in DCM, and TRPV2 may be a promising therapeutic target for advanced heart failure.
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