STATs与肝纤维化关系的研究进展

STATs and hepatic fibrosis

肝纤维化是肝脏对不同病因所致的慢性肝损伤后组织修复的代偿反应.其病理特征表现为炎性细胞募集并诱发级联反应,肝脏肌成纤细胞(myofibroblast,MFB)形成,细胞外基质(extracellular matrix,ECM)过度沉积及分布异常、正常肝结构破坏.关于肝纤维化发生的信号转导通路研究已成为目前的研究热点,其中Janus kinase/signal transducer and activator otranscription(JAK-STAT)信号通路是其中较新且近年来研究较多的一条.一般来说,STATs家族成员中STAT1和STAT5可能通过各种机制防止损伤性肝纤维化.尽管STAT2的抗病毒效果良好,但STAT2是否在促进干扰素(interferonIFN)-α/β介导的抗纤维化中也扮演了同样重要的角色目前尚不清楚.STAT3、STAT4和STAT6在肝纤维发生的生物学功能仍然不太为人所知.本文就STATs家族成员及相关细胞因子与肝纤维化研究最新进展作一综述.

Hepatic fibrosis is a response to repair of chronic hepatic injury caused by different diseases. Its pathological features are inflammatory cell aggre-gation and associated cascade reaction. There are myofibroblast formation（MFB） and excessive de-position of extracellular matrix（ECM） in the liver, and the structure of the liver is destroyed. The re-cent research finds that Janus kinase/signal trans-ducer and activator of transcription（JAK-STAT） plays an important role in the development of hepatic fibrosis. In general, STAT1 and STAT5 act as anti-fibrotic signaling molecules preventing injury-driven liver fibrosis. Although the antiviral effect of STAT2 is well documented, it is not clear whether or not STAT2 also plays a role in contrib-uting to the interferon-α/β-mediated anti-fibrotic effects in the liver. What＇s more, the biological functions of STAT3, STAT4 and STAT6 in hepatic fibrosis remains largely unknown. Therefore, this review focuses on the role of STAT family mem-bers and cytokines in hepatic fibrosis.