基于TGF-β1/Smads信号通路治疗心肌梗死后心肌纤维化的研究进展  

The research progress on treatment of myocardial fibrosis by regulating TGF-β1/Smads pathway

作　　者：石斌豪 徐宗佩[1] 樊官伟[2] 

机构地区：[1]天津中医药大学天津市现代中药重点实验室-省部共建国家重点实验室培育基地,天津300193 [2]天津中医药大学方剂学教育部重点实验室,天津300193

出　　处：《中国药理学通报》2018年第1期5-8,共4页Chinese Pharmacological Bulletin

基　　金：国家中医临床研究基地业务建设科研专项课题(No JDZX2015006)

摘　　要：心肌梗死后心肌纤维化是心脏重塑从而导致心脏衰竭的重要原因,造成心肌梗死后心室重构的机制复杂,是多因素相互作用、共同参与的结果。但其中机制较为明确,并且在心肌纤维化进程中扮演重要作用的是TGF-β1依赖的Smads信号通路。心肌梗死后,活化的TGF-β1可以通过下游Smads信号发挥持续的生物学效应,活化成纤维细胞,引起细胞外基质沉积,使心肌成纤维细胞向肌成纤维细胞分化。因此,如何阻抑或控制TGF-β1/Smads信号通路是治疗心肌梗死后心肌纤维化的重要研究方向,该文就当前基于TGF-β1/Smads信号通路治疗心肌梗死后心肌纤维化的研究进行综述。Myocardial fibrosis leads to cardiac remodeling and heart failure after myocardial infarction. The mechanism of ventricular remodeling after myocardial infarction is complicated,which results from multi-factor interactions. TGF-β1-dependent Smads signal pathway is a definite mechanism which plays an important role in the process of myocardial fibrosis. Myocardial infarction activates the TGF-β1,which links the downstream Smads signaling to play a sustained biological effects via the accumulation of activated cardiac fibroblasts and excess deposition of extracellular matrix,and the differentiation from myocardial fibroblasts to myofibroblasts. Therefore,how to block or control TGF-β1/Smads signaling pathway is an important research direction for the treatment of myocardial fibrosis after myocardial infarction. This paper reviews the current studies of the treatment of myocardial fibrosis after myocardial infarction based on the TGF-β1/Smads signaling pathway.

关 键 词：心肌梗死 心肌纤维化 TGF-Β/SMADS TGF-Β1 治疗靶点 治疗进展 

分 类 号：R-05[医药卫生] R349.1