期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 15, 期 10, 页码 19203-19225出版社
MDPI
DOI: 10.3390/ijms151019203
关键词
oxidative stress; L-type calcium channel; reactive oxygen species (ROS); glutathionylation; calcium; ROS-induced ROS release
资金
- National Health and Medical Research Council of Australia (NHMRC)
- Australian Research Council (ARC)
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.
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