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J Mol Cell Cardiol. 2014 Aug;73:112-6. doi: 10.1016/j.yjmcc.2014.02.004. Epub 2014 Feb 13.

CaMKII oxidative activation and the pathogenesis of cardiac disease.

Author information

1
Department of Internal Medicine, Division of Cardiovascular Medicine and Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, USA.
2
Department of Internal Medicine, Division of Cardiovascular Medicine and Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, USA; Department of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, USA. Electronic address: mark-e-anderson@uiowa.edu.

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".

KEYWORDS:

Arrhythmia; Ca(2+)/calmodulin dependent protein kinase II; Calcium; Heart failure; Mitochondria; Reactive oxygen species

PMID:
24530899
PMCID:
PMC4048820
DOI:
10.1016/j.yjmcc.2014.02.004
[Indexed for MEDLINE]
Free PMC Article
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