CaMKII oxidative activation and the pathogenesis of cardiac disease.

Abstract

Calcium and redox signaling both play important roles in the pathogenesis of cardiac disease; although how these signals are integrated in the heart remains unclear. One putative sensor for both calcium and oxidative stress in the heart is CaMKII, a calcium activated kinase that has recently been shown to also be regulated by oxidation. Oxidative activation of CaMKII occurs in several models of cardiac disease, including myocardial injury and inflammation, excessive neurohumoral activation, atrial fibrillation, and sinus node dysfunction. Additionally, oxidative activation of CaMKII is suggested in subcellular domains where calcium and ROS signaling intersect, such as mitochondria. This review describes the mechanism of activation of CaMKII by oxidation, the cardiac diseases where oxidized CaMKII has been identified, and suggests contexts where oxidized CaMKII is likely to play an important role. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".

• Authors: Elizabeth D Luczak, Mark E Anderson
• Journal: Journal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 73 Pg. 112-6 (Aug 2014) ISSN: 1095-8584 [Electronic] England
• PMID: 24530899 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2014 Elsevier Ltd. All rights reserved.

Chemical References

• Reactive Oxygen Species
• Calcium-Calmodulin-Dependent Protein Kinase Type 2

Topics

• Animals
• Arrhythmias, Cardiac (metabolism)
• Calcium-Calmodulin-Dependent Protein Kinase Type 2 (metabolism)
• Heart Diseases (metabolism)
• Heart Failure (metabolism)
• Humans
• Oxidation-Reduction
• Oxidative Stress (physiology)
• Reactive Oxygen Species (metabolism)