Sarcomere-based genetic enhancement of systolic cardiac function in a murine model of dilated cardiomyopathy.

ABSTRACT: Diminished cardiac contractile function is a characteristic feature of dilated cardiomyopathy (DCM) and many other heart failure (HF) causing etiologies. We tested the hypothesis that targeting the sarcomere to increase cardiac contractility can effectively prevent the DCM phenotype in muscle-LIM protein knockout (MLP^-/-) mice. The ablation of cardiac myosin binding protein C (MYBPC3^-/-) protected the MLP^-/- mice from developing the DCM phenotype. We examined the in vivo cardiac function and morphology of the resultant mouse model lacking both MLP and MYBPC3 (DKO) by echocardiography and pressure-volume catheterization and found a significant reduction in hypertrophy, as evidenced by normalized wall thickness and chamber dimensions, and improved systolic fu

SUBMITTER: Li J 

PROVIDER: S-EPMC6231975 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature