Pathophysiological role of TRPV2 as a therapeutic target for cardiomyopathy/heart failure

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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.