p38MAPK与心肌缺血/再灌注损伤的研究进展  

Research Progress of p38MAPK in Myocardial Ischemia/Reperfusion Injury

作　　者：彭晓波 梁贵友[1] PENG Xiaobo LIANG Guiyou.(Department of Cardiovascular Surgery, the Affiliated Hospital of Zunyi Medical College, Zunyi 563000, Chin)

机构地区：[1]遵义医学院附属医院心血管外科,贵州遵义563000

出　　处：《医学综述》2017年第18期3537-3541,共5页Medical Recapitulate

基　　金：国家自然科学基金(81560058;81360035;30960382);贵州省科技计划项目(黔科合SZ字2014-3022号);贵州省教育厅自然科学研究项目(黔教科合KY字2013-165号)

摘　　要：p38丝裂原活化蛋白激酶(p38MAPK)是丝裂原活化蛋白激酶家族中的重要成员,可以激活一系列发挥重要作用的细胞反应,如炎症反应及细胞的增殖、分化、凋亡和侵袭。心肌缺血/再灌注损伤(MIRI)是体外循环术后心肌损伤的重要原因,其发生不仅与氧化应激、细胞凋亡等因素有关,而且与心肌胰岛素抵抗(MIR)有关。p38MAPK不仅与心肌的氧化应激、细胞凋亡有密切的关系,在MIR中也通过影响葡萄糖转运蛋白4的表达和转位而发挥重要作用。目前,针对MIRI的发病机制采取的治疗措施均不能发挥较好的保护作用。故对p38MAPK在MIRI中的作用进一步研究,可能为p38MAPK作为预防和治疗MIRI理想的靶点提供更合理的依据。p38 mitogen activated protein kinase（p38MAPK） is an important member of the mitogen activated protein kinases family,which can activate a series to plays a critical role in cellular responses such as inflammatory response,cell proliferatian,differentiatian,apoptosis and invasion. Myocardial ischemia/reperfusion injury（MIRI） is an important cause of myocardial injury after cardiopulmonary bypass, which is related not only to oxidative stress, apoptosis and other factors, but also to myocardial insulin resistance（MIR）, p38MAPK is not only closely related to oxidative stress and apoptosis in myo- eardium, but also plays an important role in the expression and translocation of glucose transporter 4 in MIR. At present, the measures taken for the pathogenesis of MIRI cannot play a very good protective effect. Therefore, further study of the role of p38MAPK in MIRI may provide a more rational basis for p38MAPK as an ideal target for the prevention and treatment of MIRI.

关 键 词：心肌缺血/再灌注损伤 P38丝裂原活化蛋白激酶 心肌胰岛素抵抗 

分 类 号：R654[医药卫生—外科学]