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Int. J. Mol. Sci. 2014, 15(10), 19203-19225; doi:10.3390/ijms151019203

Glutathionylation of the L-type Ca2+ Channel in Oxidative Stress-Induced Pathology of the Heart

1
School of Anatomy, Physiology and Human Biology, the University of Western Australia, Crawley 6009, WA, Australia
2
Victor Chang Cardiac Research Institute, Darlinghurst 2010, NSW, Australia
*
Author to whom correspondence should be addressed.
Received: 27 August 2014 / Revised: 29 September 2014 / Accepted: 2 October 2014 / Published: 22 October 2014
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Disease 2015)
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Abstract

There is mounting evidence to suggest that protein glutathionylation is a key process contributing to the development of pathology. Glutathionylation occurs as a result of posttranslational modification of a protein and involves the addition of a glutathione moiety at cysteine residues. Such modification can occur on a number of proteins, and exerts a variety of functional consequences. The L-type Ca2+ channel has been identified as a glutathionylation target that participates in the development of cardiac pathology. Ca2+ influx via the L-type Ca2+ channel increases production of mitochondrial reactive oxygen species (ROS) in cardiomyocytes during periods of oxidative stress. This induces a persistent increase in channel open probability, and the resulting constitutive increase in Ca2+ influx amplifies the cross-talk between the mitochondria and the channel. Novel strategies utilising targeted peptide delivery to uncouple mitochondrial ROS and Ca2+ flux via the L-type Ca2+ channel following ischemia-reperfusion have delivered promising results, and have proven capable of restoring appropriate mitochondrial function in myocytes and in vivo. View Full-Text
Keywords: oxidative stress; L-type calcium channel; reactive oxygen species (ROS); glutathionylation; calcium; ROS-induced ROS release oxidative stress; L-type calcium channel; reactive oxygen species (ROS); glutathionylation; calcium; ROS-induced ROS release
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Johnstone, V.P.A.; Hool, L.C. Glutathionylation of the L-type Ca2+ Channel in Oxidative Stress-Induced Pathology of the Heart. Int. J. Mol. Sci. 2014, 15, 19203-19225.

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