肝纤维化发病机制的研究进展  

The Research Advances of the Pathogenesis of Liver Fibrosis

作　　者：高强[1] 李旭光[1] 樊莉[1] 蒋亚楠[1] 刘艳[1] 

机构地区：[1]哈尔滨医科大学药理学教研室,黑龙江哈尔滨150081

出　　处：《现代生物医学进展》2017年第14期2780-2785,2677,共7页Progress in Modern Biomedicine

摘　　要：肝纤维化(liver fibrosis,LF)是一种可由多种致病因素导致的疾病,由于尚无有效的治疗手段,其已经严重地威胁着全球人的健康。虽然LF可以逆转,但更多会发生恶化进而发展为肝硬化和肝癌。目前为止,其发病机制已经可以从多方面被阐述。肝星状细胞(hepatic stellate cells,HSCs)是LF发展的中心和关键,而其他细胞也成为影响纤维化必不可少的因素。它们以细胞因子为联系,并大量分泌首要的细胞因子-转化生长因子-β1-来刺激HSCs的激活和增殖。最终,它们共同导致胶原的沉积和细胞外基质(extracellular matrix,ECM)结构的紊乱。而这其中,长链非编码RNA也积极参与了对纤维化过程的影响。本综述将从细胞、细胞因子、ECM以及基因等方面对LF的发生和发展进行探讨,从而有助于我们明确LF的发病机制,并为研发LF有效的治疗方法提供方向。Liver fibrosis （LF）, caused by various pathogenic factors, has been seriously threatening people lives woddwide because of few effective therapy or medicine. Although LF could be reversed, it would probably progress to liver cirrhosis and cancer in most cases. The pathogenesis of LF could be expounded from many aspects, in which hepatic stellate cells （HSCs） play a pivotal and key role accompanied by other necessary cells. They communicate with each other by secreting much cytokines including transforming growth factor- β1 as a primary factor to initiate the activation and proliferation of HSCs, leading the deposition of collagen and the disorder of extracellular matrix （ECM）. In addition, long non-coding RNAs also actively participate in the progression. To help us make clear the pathogenesis of LF and provide new directions for developing more efficient therapeutic tools, the advances of pathogenesis of LF will be summarized fi：om the aspects of cells, cytokine, ECM and gene in this review.

关 键 词：肝纤维化 发病机制 治疗 

分 类 号：R575.2[医药卫生—消化系统]