Abstract
Dilated cardiomyopathy (DCM) is a common and deadly form of heart disease that is typically characterized by progressive thinning of ventricular walls, chamber dilation, and systolic dysfunction. DCM is often associated with mutations in genes encoding sarcomere or cytoskeleton proteins that confer contractile dysfunction and adverse cellular remodeling. The cytoskeletal protein Filamin C (FLNC) interacts with multiple proteins in the Z-disc and the costamere, suggesting that it contributes to costamere-based mechanotransduction in the heart.
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