心肌梗死后炎症反应研究现状  

Current situation of inflammation after myocardial infarction

作　　者：王圣洁 孙丽华[1] WANG Sheng-jie;SUN Li-hua(Department of Pharmacology,College of Pharmacy,Harbin medical University,Harbin 150086,Heilongjiang Province,China)

机构地区：[1]哈尔滨医科大学药学院药理教研室,黑龙江哈尔滨150086

出　　处：《中国临床药理学杂志》2021年第24期3374-3378,共5页The Chinese Journal of Clinical Pharmacology

基　　金：国家自然科学基金项目(81970202)。

摘　　要：炎症反应是心肌梗死(MI)后修复反应所必需的,MI后坏死细胞释放危险信号,激活固有和适应性免疫途径,引发强烈的炎症反应。Toll样受体信号转导和补体激活诱导一系列炎症细胞因子表达,诱导白细胞如中性粒细胞和单核细胞外渗至梗死心肌,促进炎症的发生发展。当梗死区浸润的中性粒细胞凋亡并被巨噬细胞吞噬后,抗炎细胞亚群逐渐占主导,激活修复细胞,促进瘢痕形成。但是梗死后炎症过度活跃、炎症反应期延长等可能会导致心肌梗死后不良重构,甚至心力衰竭。本文就心肌梗死后炎症反应过程及作用做一综述,为进一步研究MI后针对炎症反应的治疗提供参考。Inflammation is necessary for post-infarction repair. Necrotic cells activate innate and adaptive immune pathways after myocardial infarction release dangerous signals, and trigger a strong inflammatory response. Toll-like receptor signal transduction and complement activation induce the expression of a series of inflammatory cytokines, trigger leukocytes such as neutrophils and monocytes to infiltrate into the infarcted myocardium, and promote the occurrence and development of inflammation. When neutrophils infiltrated in the infarct area were apoptotic and were swallowed by macrophages, anti-inflammatory cell subsets gradually predominate the myocardium, activating repair cells and promoting the formation of scar. However, excessive inflammation after myocardial infarction and prolonged inflammatory response period may lead to poor remodeling after myocardial infarction and even heart failure. This article reviews the process and role of inflammatory response after myocardial infarction, in order to provide reference for the further study of the treatment targeting inflammatory response after myocardial infarction.

关 键 词：心肌梗死 炎症反应 免疫 心肌梗死后修复 

分 类 号：R542.22[医药卫生—心血管疾病]