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- W3200567393 endingPage "2388" @default.
- W3200567393 startingPage "2388" @default.
- W3200567393 abstract "Myocardial ischemia–reperfusion (I/R) injury significantly alters heart function following infarct and increases the risk of heart failure. Many studies have sought to preserve irreplaceable myocardium, termed cardioprotection, but few, if any, treatments have yielded a substantial reduction in clinical I/R injury. More research is needed to fully understand the molecular pathways that govern cardioprotection. Redox mechanisms, specifically cysteine oxidations, are acute and key regulators of molecular signaling cascades mediated by kinases. Here, we review the role of reactive oxygen species in modifying cysteine residues and how these modifications affect kinase function to impact cardioprotection. This exciting area of research may provide novel insight into mechanisms and likely lead to new treatments for I/R injury." @default.
- W3200567393 created "2021-09-27" @default.
- W3200567393 creator A5005886910 @default.
- W3200567393 creator A5077535251 @default.
- W3200567393 date "2021-09-11" @default.
- W3200567393 modified "2023-10-15" @default.
- W3200567393 title "Dynamic Regulation of Cysteine Oxidation and Phosphorylation in Myocardial Ischemia–Reperfusion Injury" @default.
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