Abstract

Hypertrophic and Dilated Cardiomyopathies (HCM and DCM) are caused by inherited mutations in various sarcomeric proteins. Recent advances in multiscale computational tools, coupled with multiple experiments, might expedite development of novel personalized treatments and therapeutics by quantitative assessment of how mutations alter protein activity and thus cardiac muscle contraction. Using multiscale computational platform MUSICO for precise modeling of protein-protein interactions and Ca2+ regulation in cardiac muscle, we examined the effects of potential therapeutics that modulate protein interactions and cardiac muscle contractility.

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