Cardiomyocyte Damage: Ferroptosis Relation to Ischemia-Reperfusion Injury and Future Treatment Options

Abstract

About half a century ago, Eugene Braunwald, a father of modern cardiology, shared a revolutionary belief that “time is muscle”, which predetermined never-ending effort to preserve the unaffected myocardium. In connection to that, researchers are constantly trying to better comprehend the ongoing changes of the ischemic myocardium. As the latest studies show, metabolic changes after acute myocardial infarction (AMI) are inconsistent and depend on many constituents, which leads to many limitations and lack of unification. Nevertheless, one of the promising novel mechanistic approaches related to iron metabolism now plays an invaluable role in the ischemic heart research field. The heart, because of its high levels of oxygen consumption, is one of the most susceptible organs to iron-induced damage. In the past few years, a relatively new form of programmed cell death, called ferroptosis, has been gaining much attention in the context of myocardial infarction. This review will try to summarize the main novel metabolic pathways and show the pivotal limitations of the affected myocardium metabolomics.

Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure

“…In the event of any of the emergency scenarios mentioned above, where free radicalmediated cardiomyocyte damage occurs due to hypoxia resulting from coronary artery occlusion, re-establishing a well-oxygenated blood flow by stent placement or drug treatment (thrombolytics, blood thinners, nitroglycerin, etc.) multiplies injury to the downstream cardiac cells, especially at the level of the mitochondria [23]. This damage, which is generally known as reperfusion injury, is also believed to be a consequence of elevated free radical generation in the re-perfused tissue [24].…”