Oral pharmacological inhibition of calpains attenuates isoproterenol-induced myocardial hypertrophy and fibrosis

Abstract

Background: Myocardial remodeling is an important cause of heart failure and a major medical and social problem. Our group has demonstrated that pharmacological inhibition of the Ca2+-dependent proteases calpains attenuates post-infarction remodeling and heart failure. Recent data suggest that calpain activity is elevated in non-ischemic cardiomyopathies and that G-protein coupled receptor kinase 2 (GRK2) promotes cardiac hypertrophy. Objective: To determine the therapeutic benefit and mechanism of inhibiting calpain activity in pathological myocardial remodeling of non-ischemic cause.