UC Davis

The Ca²⁺-calmodulin dependent protein kinase II (CaMKII) is an established central mediator of electrophysiological and contractile responses to cardiac stress, and its hyper-activation in cardiac diseases has been linked to heart failure (HF) and arrhythmia. Here we summarize the evidence supporting the role of CaMKII as a critical nodal point for therapeutic intervention against HF and atrial and ventricular tachyarrhythmias. Targeting of CaMKII in heart with inhibitors possessing appropriate selectivity might represent a novel therapeutic approach for HF and arrhythmias.