Caveolin-1 Modulates Cardiac Gap Junction Homeostasis and Arrhythmogenecity by Regulating cSrc Tyrosine Kinase

Abstract

The present studies reveal the critical role of Cav1 in modulating cSrc activation, gap junction remodeling, and ventricular arrhythmias. These data provide a mechanistic explanation for the observed genetic link between Cav1 and cardiac arrhythmias in humans and suggest that targeted regulation of Cav1 may reduce arrhythmic risk in cardiac diseases associated with renin-angiotensin system activation.