AngⅡ诱导的心肌纤维化中心肌成纤维细胞增殖调控机制的研究进展  

Research Progress in Regulation Mechanism of AngⅡ-induced Cardiac Fibroblasts Proliferation in Myocardial Fibrosis

作　　者：白丽平 田海萍[1] 刘艳阳[1] BAI Liping;TIAN Haiping;LIU Yanyang(Department of Cardiology,Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010050,China)

机构地区：[1]内蒙古医科大学附属医院心内科,呼和浩特010050

出　　处：《医学综述》2022年第19期3781-3788,共8页Medical Recapitulate

基　　金：内蒙古自治区自然科学基金(2020MS08142);内蒙古自治区高等学校科学研究项目(NJZZ2019)。

摘　　要：心肌纤维化是心血管疾病的重要病理过程,由其导致的不良心血管事件逐年增加。心肌成纤维细胞是心肌纤维化的首要效应细胞,血管紧张素Ⅱ作为致心肌纤维化的重要因子,负责调控心肌成纤维细胞的增殖、分化和细胞外基质的沉积。其调控机制复杂,可能涉及信号转导及转录活化因子3、Ras同源基因家族成员A、p38促分裂原活化的蛋白激酶、瞬时受体电位等信号通路以及转化生长因子-β_(1)、结缔组织生长因子、血清反应因子等细胞因子。因此,从分子层面上了解各信号转导通路及细胞因子调控心肌纤维化的机制有利于实现心肌纤维化的三级预防,提高心脏病患者的远期预后。Myocardial fibrosis is an important pathological process of many cardiovascular diseases,the adverse vascular events caused by which are increasing year by year.Myocardial fibroblasts are the primary effector cells of myocardial fibrosis.As an important factor of myocardial fibrosis,angiotensinⅡis responsible for regulating the proliferation,differentiation and extracellular matrix deposition of cardiac fibroblasts.The regulation mechanism is complex and diverse,which may be related to the signal transducer and activator of transcription 3 signal pathway,Ras homolog family member A signal pathway,p38 mitogen activated protein kinase signal pathway,transient receptor potential signal pathway and transforming growth factor-β_(1),connective tissue growth factor,serum reaction factor,,etc.Therefore,understanding the signaling pathways and cytokines regulating myocardial fibrosis at the molecular level is conducive to achieving tertiary prevention of myocardial fibrosis and improving the long-term prognosis of the cardiac patients.

关 键 词：心肌纤维化 血管紧张素Ⅱ 心肌成纤维细胞 调控机制 

分 类 号：R542.2[医药卫生—心血管疾病]