肝纤维化发病机制与治疗进展  

Pathogenesis and advances in treatment of liver fibrosis

作　　者：林沪[1] 陈黎明[1] 叶文华[1] 李元元[1] 耿华[1] 王福生[1] 

机构地区：[1]解放军第三0二医院感染六科,北京100039

出　　处：《国际流行病学传染病学杂志》2009年第5期324-327,共4页International Journal of Epidemiology and Infectious Disease

基　　金：国家杰出青年科学基金（30525042）

摘　　要：细胞外基质（ECM）的合成增加和降解减少是肝纤维化形成的主要机制，肝星形细胞（HSC）活化是肝纤维化形成的细胞学基础。去除病因，抗炎，抑制HSC活性与增殖，刺激活化HSC凋亡，促进ECM降解均为抗肝纤维化治疗的标靶。间充质干细胞移植抗纤维化尚有争议。基质金属蛋白酶（MMP）基因转导系统因可调控性及安全性问题，用于临床尚需时日。该文就肝纤维化发病机制与治疗进展作了综述。The main mechanism of liver fibrosis is the unbalance of synthesis and degradation of extracellular matrix. Hepatic stellate cell is the main source of extracellular matrix. Removal of underling stimulus, anti-inflammatory, suppressing the activation and proliferation of hepatic stellate cells, stimulating the apoptosis of activated hepatic stellate cells, promoting the degradation of extracellular matrix would be the therapic targets of liver fibrosis. The transplantation of mesenchymal stem cells as an anti-fibrotic therapy is in controversy. The gene delivery of matrix metalloproteinase can not be used on clinic as its regulation and safety is still in doubt. In tiffs article, the patliogenesis and treatment progress of liver fibrosis are reviewed.

关 键 词：肝硬化 细胞外基质 肝星形细胞 

分 类 号：R575.2[医药卫生—消化系统] R722.12[医药卫生—内科学]