05182022Wed
Last updateWed, 09 Mar 2022 4am

Clinical manifestations and basic mechanisms of myocardial ischemia/reperfusion injury

Chiu‑Fen Yanga,b,c*

aDepartment of Cardiology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan, bDoctoral Degree Program in Translation Medicine, Tzu Chi University and Academia Sinica, Hualien, Taiwan, cInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan

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Open Access funded by Buddhist Compassion Relief Tzu Chi Foundation

 

 

Abstract
Acute myocardial ischemia/reperfusion (I/R) injury is a significant, unsolved clinical puzzle. In the disease context of acute myocardial infarction, reperfusion remains the only effective strategy to salvage ischemic myocardium, but it also causes additional damage. Myocardial I/R injury is composed of four types of damage, and these events attenuate the benefits of reperfusion therapy. Thus, inventing new strategies to conquer I/R injury is an unmet clinical need. A variety of pathological processes and mediators, including changes in the pH, generation of reactive oxygen radicals, and intracellular calcium overload, are proposed to be crucial in I/R‑related cell injury. Among the intracellular events that occur during I/R, we stress the importance of protein phosphorylation signaling and elaborate its regulation. A variety of protein kinase pathways could be activated in I/R, including reperfusion injury salvage kinase and survivor‑activating factor enhancement pathways, which are critical to cardiomyocyte survival. In addition to serine/threonine phosphorylation signaling, protein tyrosine phosphorylation is also critical in multiple cell functions and survival. However, the roles of protein kinases and phosphatases in I/R have not been extensively studied yet. By better understanding the mechanisms of I/R injury, we may have a better chance to develop new strategies for I/R injury and apply them in the clinical patient care.


Keywords: Acute myocardial infarction, Ischemia/reperfusion injury, Protein phosphorylation

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