肝纤维化是由急性或持续的肝损害慢性化而始动,继之以炎性细胞游走、枯否细胞激活,导致贮脂细胞(Ito细胞)增生、转化和分裂,从而使胶原合成增多,蛋白多糖、透明质酸、结构性糖蛋白等细胞外基质水平提高的动态发展过程.最近的大量研究表明,肝纤维化存在着高度复杂的病理生化反应,肝实质细胞与非实质细胞及它们与周围细胞外基质构成的网络,还有多种信号介导的并成为生长因子海绵样接受容器(sponge-Likereservoir of growth factors)的靶细胞都参与了 Hepatic fibrosis is initiated by chronic or chronic liver damage followed by inflammatory cell migration and activation of Kupffer cells, resulting in proliferation, transformation and division of the storage fat cells (Ito cells), resulting in increased collagen synthesis , Proteoglycans, hyaluronic acid, structural glycoproteins and other extracellular matrix levels of the dynamic development of a large number of recent studies have shown that there is a highly complex liver fibrosis pathological and biochemical reactions, liver parenchymal cells and non-parenchymal cells and their Networks with the surrounding extracellular matrix, as well as a variety of signal-mediated target cells that are sponge-like reservoir of growth factors, are involved