Abstract
Mutations in the muscle specific intermediate filament protein desmin lead to cardiomyopathy. Desmin deficient mice (des−/−) show defects in all muscle types, the most prominent being the heart which develops dilated cardiomyopathy due to cardiomyocyte cell death. By the second week of their lifetime the hearts of des−/− mice are extensively infiltrated by inflammatory cells. Acute inflammation is gradually regressed, followed by a less dynamic remodeling phase characterized by collagen deposition and scar formation.
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