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The molecular biology of dilated cardiomyopathy

N.E. Bowles1

Department of Pediatrics (Cardiology), Baylor College of Medicine, Houston, Texas, U.S.A.

1 Correspondence: Neil E. Bowles, PhD, Department of Pediatrics (Cardiology), Baylor College of Medicine, One Baylor Plaza, Room 333E, Houston, TX 77030, U.S.A.

Abstract

Cardiomyopathies are disorders affecting heart muscle which usually result in inadequate pumping of the heart and are the most common cause of heart failure. Dilated cardiomyopathy (DCM) causes ventricular dilation and dysfunction, primarily of the left ventricle, and has many etiologies. Genetic heterogeneity exists and several of these genes are now known, including dystrophin, cardiac actin, desmin, {delta}-sarcoglycan, cardiac troponin T, ß-myosin heavy chain, {alpha}-tropomyosin, titin and metavinculin. Here I will review the identification of genes associated with DCM and data demonstrating that dystrophin may provide a common pathway in the pathogenesis of cardiomyopathies.

Key Words: Genetics • cardiomyopathy • cytoskeleton

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