p38MAPK在心力衰竭发病机制中的研究进展  

Research Progress of the Role of p38MAPK in the Pathogenesis of Heart Failure

作　　者：王淑香[1,2] 赵强[1,2] 

机构地区：[1]暨南大学第四附属医院 [2]广州市红十字会医院心血管内科,广州510220

出　　处：《医学综述》2014年第19期3486-3488,共3页Medical Recapitulate

摘　　要：p38促分裂原活化的蛋白激酶(p38MAPK)是一种可被应激源激活的蛋白酶,目前已被证实能在人类的心脏中表达,并在心力衰竭(心衰)的发展机制中担任着重要的角色。该文就p38MAPK近年来在心衰机制中的研究进展(包括心脏重构、心肌纤维化以及与β肾上腺素能受体的关系)进行综述,以更直观地了解p38MAPK在心衰发展过程中的作用,为p38MAPK作为理想的靶点提供更合理的依据,并对将来如何寻找潜在机制链中的关键点提出展望。The p38 mitogen-activated protein kinases（p38MAPKs） are stress-actived proteins that have been demonstrated to be activated in the human heart and play an important role in the heart failure.Here focuses on the latest advances in p38 MAPK involvement in the mechanisms of cardiac remodeling,myocardial fibrosis,and the association with the β-adrenergic receptors.It directly reveals the role of p38MAPK in the progression of heart failure and provides the basis for the targeting of p38MAPK,as well as the future direction of discovering the underlying key point in the mechanism chain of heart failure.

关 键 词：p38促分裂原活化的蛋白激酶 心力衰竭 心脏重构 心肌纤维化 Β肾上腺素能受体 

分 类 号：R541.61[医药卫生—心血管疾病]