细胞因子信号转导抑制分子-3在肝纤维化中的作用及研究进展

Research progress of role of SOCS-3 in treating liver fibrosis

肝纤维化是继发于各种慢性肝损伤之后组织修复过程中的代偿反应,其发病实质是肝内细胞外基质(extracellular matrix,ECM)合成与降解动态平衡发生紊乱,最终导致ECM过度沉积。肝纤维化的发生与发展受到多种细胞因子及细胞内多种信号转导通路网络的调控,其中很多靶点在肝纤维化中的作用尚没有完全定论。近年来越来越多的研究证实细胞因子信号转导抑制分子-3(suppressor of cytokine signaling,SOCS-3)在肝纤维化的发生与发展过程中扮演着重要角色。SOCS-3可通过调控肝脏内炎症反应、细胞增殖活化、胰岛素抵抗、瘦素抵抗等影响肝脏疾病的发展进程。许多学者认为SOCS-3可作为肝纤维化疾病诊断、预测预后的生物分子指标以及治疗靶标。该文从SOCS-3系统概述、SOCS-3与肝纤维化关系、SOCS-3在防治肝纤维化中的作用等方面综述了SOCS-3在防治肝纤维化中的作用及研究进展。

Liver fibrosis occurs as compensatory responses to tissue repairing process in a wide range of chronic liver injures. It is characterized by excessive deposition of extracellular matrix( ECM) in liver tissues. The new discovery shows that suppressor of cytokine signaling( SOCS-3) is strictly associated with fibrogenic progression of chronic liver diseases. Recent basic and clinical investigations also demonstrate that liver fibrogenesis is accompanied by SOCS-3,which critically determines the pathogenesis and prognosis of liver fibrosis. This review summarizes current knowledge on SOCS-3 and the relationships between SOCS-3 and liver fibrosis. On the other hand,it also presents the different strategies that have been used in experimental models to counteract excessive SOCS-3 and the role of SOCS-3 in the prevention and treatment of liver fibrosis.