🤖This page has been translated by AI and may contain inaccuracies. Please refer to the original content for clarification.

Role of N6-adenosine Methylation in Myocardial Ischemia-Reperfusion Injury and Research Progress
Abstract:Acute myocardial infarction is caused by occlusion of the coronary artery, leading to myocardial ischemia and infarction, and has become one of the main causes of death among residents in China [1]. After acute myocardial infarction, thrombolytic therapy, percutaneous coronary intervention, and coronary stent placement are the preferred methods to restore blood supply, reduce the infarct size, and salvage the myocardium. Although these treatments effectively reduce the mortality rate of myocardial infarction, reperfusion can cause metabolic dysfunction, irreversible structural and functional damage to the myocardium, known as myocardial ischemia-reperfusion injury (MIRI), which may lead to serious complications such as heart failure, myocardial fibrosis, arrhythmia, and sudden death [2].
Keywords:Myocardial Reperfusion InjuryAutophagyApoptosisPyroptosisFerroptosisN6-Adenosine Methylation
Publication Date:2025-05-15
Online Publishing Date:2025-08-15(First online date of this platform, not the publication date of the document)
Pages:4( 666-669 )