随着医疗技术的不断进步,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,当缺血心肌细胞的血流恢复之后,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,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,炎症反应在心肌再灌注损伤中扮演着关键角色,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,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。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.
铁死亡是一种依赖于铁离子与活性氧(reactiveoxygen species, ROS)诱导的脂质过氧化物积累,进而引发的一种特殊的细胞死亡机制,是一种调节性细胞死亡的形式。近年来研究显示,其在肿瘤、心脏、肾脏、脑的缺血再灌注损伤及其他多种疾病中发挥重要作用。本文将从铁代谢、脂质代谢、氨基酸代谢等机制方面综述铁死亡在心肌缺血再灌注损伤中的研究进展。并总结了可能对心肌缺血再灌注损伤有治疗作用的抑制剂及相关靶点,旨在从铁死亡角度为治疗心肌缺血再灌注损伤提供新的防治策略。Ferroptosis is a special mechanism of cell death induced by the accumulation of lipid peroxides, which depends on iron ions and reactive oxygen species (ROS). It is a form of regulated cell death. In recent years, research has shown that it plays an important role in tumors, cardiac, renal, cerebral ischemia-reperfusion injury, and many other diseases. This paper reviews the research progress of ferroptosis in myocardial ischemia-reperfusion injury from the aspects of mechanisms such as iron metabolism, lipid metabolism, and amino acid metabolism. It also summarizes the inhibitors and related targets that may have a therapeutic effect on myocardial ischemia-reperfusion injury, aiming to provide new prevention and treatment strategies for myocardial ischemia-reperfusion injury from the perspective of ferroptosis.
