论文部分内容阅读
肝纤维化是多种慢性肝病发展至肝硬化的必由之路。慢性肝损伤后,以胶原为主的细胞外基质(ECM)成分合成增多,降解相对不足,过多胶原沉积在肝内引起肝纤维化。同时肝纤维化的形成和发展是一个涉及多细胞的过程。现已证明肝星状细胞(HSC)的激活是肝纤维化发生的核心环节,因为激活的HSC是合成ECM的主要细胞。慢性肝损害后,HSC被激活成一种新表型,表现为增殖、活动、收缩及ECM成分合成增多,从而为组织修复过程中ECM网络的重建提供重要支持。很多因素对HSC激活起促进作用,包括ECM组成及结构的广泛改变,数种生长因子、细胞因子、趋化因子、氧化反应产
Liver fibrosis is the only way to develop a variety of chronic liver diseases to cirrhosis. After chronic liver injury, collagen-based extracellular matrix (ECM) component synthesis increased, the relative lack of degradation, excessive collagen deposition in the liver caused by liver fibrosis. At the same time, the formation and development of liver fibrosis is a multi-cellular process. It has been demonstrated that activation of hepatic stellate cells (HSCs) is central to the development of hepatic fibrosis, as activated HSCs are the major cells that synthesize ECMs. After chronic liver damage, HSC is activated into a new phenotype, showing proliferation, activity, contractions and increased synthesis of ECM components, thus providing an important support for the reconstruction of ECM network during tissue repair. A number of factors contribute to HSC activation including extensive changes in the composition and structure of ECMs, several growth factors, cytokines, chemokines, and oxidative responses