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.
Highlights
IntroductionMyocardial ischemia–reperfusion (I/R) injury often precedes more severe forms of cardiovascular disease (i.e., heart failure) [1]
Dynamic Regulation of CysteineMyocardial ischemia–reperfusion (I/R) injury often precedes more severe forms of cardiovascular disease [1]
This study demonstrates that possible Akt oxidation in the heart may lead to inactivation and greater I/R injury
Summary
Myocardial ischemia–reperfusion (I/R) injury often precedes more severe forms of cardiovascular disease (i.e., heart failure) [1]. While studies have strived to reduce I/R injury, clinical treatments have failed to drastically reduce cell death and preserve myocardium. Significant progress has been made to understand the molecular underpinnings of cardioprotection in preclinical models and some hope remains to effectively reduce I/R injury. Reduction–oxidation (redox) reactions are crucial processes that help maintain cardiac homeostasis and are known to regulate cell signaling pathways. This review aims to summarize important, recent work studying the cysteine oxidation of kinases essential to cardioprotection and highlight an emerging area of research. Novel studies are needed to further understand the molecular processes that govern cardiac homeostasis and protection. Harnessing and exploiting these pathways may provide a road for new therapeutics.
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