肝纤维化是肝损伤的修复机制。肝星状细胞表型转换和增生在肝纤维化形成中起重要作用。通过TNF超家族受体Fas及P75、外周苯二氮卓类受体PBR、整合素受体介导激活的肝星状细胞凋亡而使其数量减少 ,细胞外基质和基质金属蛋白酶组织抑制因子明显下降 ,从而导致肝纤维化发生逆转。肝星状细胞的凋亡受到凋亡和抗凋亡基因、细胞因子等的调控。表明可通过调节肝星状细胞的凋亡为治疗肝纤维化寻找理想途径。 Liver fibrosis is a repair mechanism of liver injury. Hepatic stellate cell phenotype conversion and proliferation plays an important role in the formation of hepatic fibrosis. Through TNF superfamily receptor Fas and P75, peripheral benzodiazepine receptor PBR, integrin receptor-mediated activation of hepatic stellate cell apoptosis and to reduce the number of extracellular matrix and matrix metalloproteinase tissue inhibitor of Significantly decreased, leading to reversal of liver fibrosis. Apoptosis of hepatic stellate cells is regulated by apoptosis and anti-apoptotic genes, cytokines and the like. It is indicated that an ideal route for the treatment of liver fibrosis can be found by regulating the apoptosis of hepatic stellate cells.