Non-ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use?

J Mol Cell Cardiol. 2018 Aug:121:300-303. doi: 10.1016/j.yjmcc.2017.10.010. Epub 2017 Oct 25.

Abstract

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.

Keywords: Arrhythmia; Atrial fibrillation; CaMKII; Heart failure; Small molecules.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Atrial Fibrillation / drug therapy*
  • Atrial Fibrillation / genetics
  • Atrial Fibrillation / pathology
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / antagonists & inhibitors
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics*
  • Heart Failure / drug therapy*
  • Heart Failure / genetics
  • Heart Failure / pathology
  • Humans
  • Molecular Targeted Therapy
  • Myocytes, Cardiac

Substances

  • Calcium-Calmodulin-Dependent Protein Kinase Type 2