Molecular mechanism of contractile dysfunction and the alteration of intracellular Ca^<2+> handling caused by mutation of cardiac troponin T

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We explored the mechanism of pathogenesis and sudden death in dilated cardiomyopathy using knock-in mouse model with mutant troponin T (DCM mouse). DCM mouse died suddenly from age of 1 month old. In DCM mouse, cardiac chamber was dilated and contractile functions were impaired. A blocker of angiotensin II receptor (ARB) significantly increased survival rate and improved the cardiac functions without changing the decreased Ca^<2+> sensitivity in DCM mouse. ARB also improved the fibrosis and electrocardiogram, which were considered as critical for the beneficial effects of ARB.