Dynamic Regulation of Cysteine Oxidation and Phosphorylation in Myocardial Ischemia–Reperfusion Injury

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.

The Role of Pyroptosis and Autophagy in Ischemia Reperfusion Injury

“…Myocardial I/R injury is a disease that leads to myocardial dysfunction, structural damage, and electrical activity disorder after the recovery of coronary blood flow in ischemic heart disease. It leads to a notable increase in the death rate of myocardial infarction and has become one of the main risk factors threatening human health [ 79 , 80 ]. Si-Miao-Yong-An decoction (SMYAD) is a kind of traditional Chinese medicine that is mainly used to clear away heat, detoxify, promote blood circulation, and relieve pain [ 81 ].…”

LOXL1-AS1 Aggravates Myocardial Ischemia/Reperfusion Injury Through the miR-761/PTEN Axis

“…Myocardial ischemia and reperfusion injury (MIRI) is the pathological process leading to the death of cardiomyocytes, which significantly changes heart function after infarction and increases heart failure risk. 1) MIRI induces sterile injury and inflammation and is characterized by the release of DAMPs, thereby initiating and triggering NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasomes. 2) Despite advances in cardiovascular medicine, MIRI still increases mortality and lengthens hospital stays.…”

Modulation of Inula racemosa Hook Extract on Cardioprotection by Ischemic Preconditioning in Hyperlipidaemic Rats

“…Endothelial dysfunction, oxidative stress, and apoptosis–necrosis–inhibition have been linked to I/R-induced damage. An endogenous technique for protecting the ischemic heart is ischemia preconditioning (IPC) [ 2 ], which can mitigate these effects [ 3 , 4 ]. However, during the IPC, the myocardium undergoes a brief but potentially fatal bout of sublethal ischemia and reperfusion [ 5 ].…”