Bedossa Pierre, Paradis Valérie
Service d'Anatomie Pathologique, CNRS FRE2443, Hôpital de Bicêtre, 78 Avenue Géneral Leclerc, 94275 Le Kremlin-Bicêtre, France.
J Pathol. 2003 Jul;200(4):504-15. doi: 10.1002/path.1397.
Liver fibrosis is the hallmark of every chronic liver disease. It is also the major factor of morbidity and mortality due to the development of cirrhosis and its complications including hepatocellular carcinoma. But even at the beginning of the process of liver fibrosis and due to the strategic position of the extracellular matrix at the interface between blood flow and epithelial compartment, any quantitative or qualitative modification of extracellular matrix will rapidly affect structure and function of the liver. The development of several animal models of liver fibrosis as well as isolation and cultivation of hepatic stellate cells, the major fibrogenic cell type in the liver, led to the gathering of recent knowledge on the mechanism of liver fibrosis. Activation of hepatic stellate cells is a key event in this process and many details on this finely tuned mechanism are now available. In addition to these experimental data, experience from chronic hepatitis C now allows the development of new concepts and perspectives such as liver fibrosis regression and antifibrotic therapies.
肝纤维化是所有慢性肝病的标志。它也是因肝硬化及其并发症（包括肝细胞癌）的发展而导致发病和死亡的主要因素。但即使在肝纤维化过程的初期，由于细胞外基质在血流与上皮腔室之间界面处的关键位置，细胞外基质的任何定量或定性改变都会迅速影响肝脏的结构和功能。多种肝纤维化动物模型的建立以及肝脏主要纤维化细胞类型肝星状细胞的分离和培养，使人们对肝纤维化机制有了最新认识。肝星状细胞的激活是这一过程中的关键事件，目前关于这一精细调节机制的许多细节已为人所知。除了这些实验数据外，慢性丙型肝炎的治疗经验现在也催生了诸如肝纤维化消退和抗纤维化治疗等新的概念和观点。
