%0 Journal Article
%T 炎症反应在心肌缺血再灌注损伤中的研究进展<br>Research Progress on Inflammatory Response in Myocardial Ischemia-Reperfusion Injury
%A 杜智威
%A 刘振兵
%J Advances in Clinical Medicine
%P 1944-1952
%@ 2161-8720
%D 2025
%I Hans Publishing
%R 10.12677/acm.2025.153823
%X 随着医疗技术的不断进步&#65292;溶栓和经皮冠状动脉介入等治疗手段显著降低了急性心肌梗死的死亡率。然而&#65292;当缺血心肌细胞的血流恢复之后&#65292;随之而来的心肌再灌注损伤却可能进一步加重心肌损伤。心肌再灌注损伤的机制复杂多样&#65292;主要包括钙超载、炎症反应、氧化应激、内皮功能障碍、免疫反应、线粒体功能障碍、心肌细胞凋亡、自噬和细胞焦亡等。其中&#65292;炎症反应在心肌再灌注损伤中扮演着关键角色&#65292;抑制炎症反应可以有效减轻心肌再灌注损伤。文章重点介绍炎症在心肌再灌注损伤中的作用机制&#65292;为提升心肌再灌注损伤的临床治疗效果和改善患者预后提供新的策略。<br>With the continuous advancement of medical technology, treatment methods such as thrombolysis and percutaneous coronary intervention have significantly reduced the mortality rate of acute myocardial infarction. However, after the blood flow to ischemic myocardial cells is restored, the subsequent myocardial reperfusion injury may further exacerbate myocardial damage. The mechanisms of myocardial reperfusion injury are complex and diverse, mainly including calcium overload, inflammatory response, oxidative stress, endothelial dysfunction, immune response, mitochondrial dysfunction, myocardial cell apoptosis, autophagy, and pyroptosis. Among them, the inflammatory response plays a crucial role in myocardial reperfusion injury, and inhibiting the inflammatory response can effectively alleviate myocardial reperfusion injury. This article focuses on introducing the mechanism of action of inflammation in myocardial reperfusion injury, aiming to provide new strategies for improving the clinical treatment effect of myocardial reperfusion injury and the prognosis of patients.
%K 缺血再灌注损伤&#65292
%K 炎症&#65292
%K 细胞焦亡&#65292
%K 通路<br>Ischemia-Reperfusion Injury
%K Inflammation
%K Pyroptosis
%K Pathway
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=109848