Key result
Old mdx mice exhibited raised resting intracellular Ca(2+) concentrations and abnormal Ca(2+) transients, which were reduced by stretch-activated channel inhibitors.
Population
Single ventricular myocytes and whole hearts from young and old mdx mice and wild-type mice
Comparison
Stretch-activated channel inhibitors vs Wild-type mice and untreated mdx mice
Design
Preclinical
Authors
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Hypothesis-generating for SAC inhibition in dystrophic cardiomyopathy; leaves open clinical translation in Duchenne muscular dystrophy.
Stretch-activated channels may underlie abnormal calcium handling and contribute to the pathogenesis of heart failure in Duchenne muscular dystrophy.
Williams et al. (2006) studied Duchenne muscular dystrophy. mdx mutation (absence of dystrophin) vs. wild-type mice was evaluated on Intracellular Ca(2+) concentration and Ca(2+) transients. Old mdx mice exhibited raised resting intracellular Ca(2+) concentrations and abnormal Ca(2+) transients, which were reduced by stretch-activated channel inhibitors.
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