Abstract
Disruption of dystrophin–glycoprotein complex caused by genetic defects of dystrophin or sarcoglycans results in muscular dystrophy and/or cardiomyopathy in human and animal models. Abnormal Ca2+ handling has been thought to be a key molecular event in the pathology of these diseases. However, the detailed mechanism for Ca2+ abnormality remains elusive. We have previously shown that the transient receptor potential cation channel TRPV2 is a principal candidate for Ca2+-entry pathways in dystrophic muscles.
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