TMEM16A Plays an Insignificant Role in Myocardium Remodeling but May Promote Angiogenesis of Heart During Pressure-overload.

ABSTRACT: Background: Cardiac hypertrophy (CH) occurs with an increase in myocardium mass as an adaptive compensation to increased stress. Prolonged CH causes decompensated heart failure (HF). Enhanced angiogenesis by vascular endothelial growth factor (VEGF) is observed in hypertrophied hearts; impaired angiogenesis by angiotensin II (AngII) is observed in failing hearts. Angiogenesis is executed by vascular endothelial cells (ECs). Abnormal Ca²⁺ homeostasis is a hallmark feature of hypertrophied and failing hearts. Ca²⁺-activated chloride channel transmembrane protein 16A (TMEM16A) is expressed in cardiomyocytes and ECs but its role in heart under stress remains unknown. Methods: Pressure-overload-induced CH and HF mouse models were established. Echocardiography

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC9194855 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature