Ca2+/Calmodulin-Dependent Protein Kinase II Equally Induces Sarcoplasmic Reticulum Ca2+ Leak in Human Ischaemic and Dilated Cardiomyopathy

Abstract

Functional and molecular measures of the SR Ca(2+) leak are comparable in human ICM and DCM. CaMKII is equally responsible for the induction of the 'RyR2 leakiness' in both pathologies. Thus, CaMKII inhibition as a therapeutic measure may not be restricted to patients suffering from DCM but rather may be beneficial for the majority of HF patients.