Glutathionylation of the L-type Ca2+ Channel in Oxidative Stress-Induced Pathology of the Heart
AbstractThere 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
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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.
Johnstone VPA, Hool LC. Glutathionylation of the L-type Ca2+ Channel in Oxidative Stress-Induced Pathology of the Heart. International Journal of Molecular Sciences. 2014; 15(10):19203-19225.Chicago/Turabian Style
Johnstone, Victoria P.A.; Hool, Livia C. 2014. "Glutathionylation of the L-type Ca2+ Channel in Oxidative Stress-Induced Pathology of the Heart." Int. J. Mol. Sci. 15, no. 10: 19203-19225.