丝裂原活化蛋白激酶通路在心肌缺血/再灌注损伤中的作用机制及药物防治  

Exploring the mechanism and drug prevention and treatment of myocardial ischemia/reperfusion injury based on mitogen-activated protein kinase pathway

作　　者：陶婷 邹琦 韩国栋 孙守刚[2] TAO Ting;ZOU Qi;HAN Guodong;SUN Shougang(The Second Clinical College of Lanzhou University,Lanzhou,Gansu 730030,China;Department of Cardiology,Lanzhou University Second Hospital,Lanzhou,Gansu 730030,China)

机构地区：[1]兰州大学第二临床医学院,甘肃兰州730030 [2]兰州大学第二医院心血管内科,甘肃兰州730030

出　　处：《安徽医药》2025年第5期862-868,共7页Anhui Medical and Pharmaceutical Journal

基　　金：甘肃省科技重点研发计划(22YF7FA088);兰州大学第二医院“萃英科技创新”计划(CY2021-MS-B14)。

摘　　要：目前,心肌梗死(MI)的发病率和死亡率不断上升。其主要治疗方法包括经皮冠状动脉介入术、冠状动脉搭桥术和溶栓治疗。尽管上述治疗提高了心肌存活率,但它们也增加了心肌缺血/再灌注损伤(MIRI)的风险。丝裂原活化蛋白激酶(MAPK)通路与心肌细胞凋亡、自噬和线粒体功能障碍密切相关,在缺血/再灌注(I/R)损伤的发生发展中扮演着重要的角色。近年来众多研究显示,通过药物调控MAPK通路可以有效缓解MIRI。然而,目前仍缺乏该领域的系统性描述,现总结MAPK通路在MIRI中的作用机制及相关的靶向治疗药物,为MIRI的防治提供理论依据。Currently,the incidence and mortality rate of myocardial infarction(MI)are on the rise.The main treatment methods include percutaneous coronary intervention,coronary artery bypass grafting,and thrombolytic therapy.Although the above treatments have increased myocardial survival rates,they also elevate the risk of myocardial ischemia/reperfusion injury(MIRI).The Mitogen-activated protein kinase(MAPK)pathway is closely associated with myocardial cell apoptosis,autophagy,and mitochondrial dysfunction,playing a significant role in the occurrence and development of ischemia/reperfusion(I/R)injury.In recent years,numerous studies have shown that drug modulation of the MAPK pathway can effectively alleviate myocardial ischemia/reperfusion injury.However,there is still a lack of systematic description in this field.This study aims to provide a theoretical basis for the prevention and treatment of MIRI by summarizing the mechanisms of action of the MAPK pathway in MIRI and related targeted therapeutic drugs.

关 键 词：心肌再灌注损伤 丝裂原活化蛋白激酶通路 作用机制 药物防治 

分 类 号：R541.4[医药卫生—心血管疾病] R542.2[医药卫生—内科学]