血管紧张素Ⅱ及其受体AT1R与肝纤维化的相关性

Relation of angiotensin Ⅱ and its receptor AT1R with liver fibrosis

肝纤维化是各种慢性肝损伤修复过程引起的肝脏疾病,以细胞外基质(extracellular matrix,ECM)增生和降解失衡导致过度沉积为特征。血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)是肾素血管紧张素系统(renin-angiotensin system,RAS)中的主要效应成分。越来越多的证据表明,AngⅡ及其1型受体(angiotensin receptor 1,AT1R)之间的相互作用在对长期肝脏损伤引起的纤维化中起重要作用,包括促进肝星状细胞(hepatic stellate cell,HSC)的活化、增殖及收缩,诱导人类活化型HSCs产生活性氧簇(reactive oxygen species,ROS),促进胶原合成及沉积等。本文就AngⅡ及其受体AT1R在肝纤维化的发生、发展及抗纤维化治疗中的作用作一综述。

Hepatic fibrosis is a common disease caused by wound-healing response to a variety of chronic liver injuries;it is characterized by the imbalance of extracellular matrix synthesis and degradation.Angiotensin Ⅱis the major effector of the renin-angiotensin system.Increasing evidence has demonstrated that the interaction of angiotensinⅡ with angiotensin receptor 1plays an important role in the long-term liver injury-induced liver fibrosis by inducing the activation,proliferation and constriction of hepatic stellate cells,generation of the reactive oxygen species from activated hepatic stellate cells,and the synthesis and accumulation of collagen.In this article we focused on the role of angiotensin Ⅱ and its receptor 1in the pathogenesis,development and therapy of liver fibrosis in recent years.