[Regulatory effects of microRNAs on hepatic stellate cell activation and liver fibrogenesis].

Hepatic fibrogenesis (HF) is the common consequence of various chronic liver diseases (CLD) induced by a variety of pathogenic factors. The mechanism of HF involves the interactions within different types of liver cells, cytokines, chemokines, cell mediators and multiple signaling pathways in a way of networks. As a result, excessive production and deposition of extracellular matrix (ECM) mainly composed of type I and type III fibril forming collagen destroys the original morphology, structure and function of the liver. The activation of hepatic stellate cells (HSCs), the major scar forming cells in liver, plays a crucial role in hepatic fibrogenesis. MicroRNAs are a group of short, single stranded, non-coding RNAs that can inhibit mRNA expression at the transcriptional and post transcriptional levels. They can be loaded and transferred as cargos by exosomes, to regulate the function of nearby and distant receptive cells. The expressions of many microRNAs such as miR-21, miR-29, miR-708, miR-101, miR-455, miR-146, miR-193 change significantly in activated HSCs, which regulate the activation, fibrogenic function, proliferation, apoptosis and autophagy of HSCs via affecting target genes expression and signaling pathway molecules. They are important substances and regulatory mechanism that mediate the initiation and progression of HF.肝纤维化是各种病因引起的慢性肝病的共同转归。肝纤维化的发生是各类肝脏细胞、细胞因子、趋化因子、细胞介质相互作用的结果，并通过活化多种信号通路和转录因子，导致肝脏内以I、III型纤维形成性胶原为主的细胞外基质的过度产生和沉积，最终破坏肝脏组织原有的形态、结构和功能。其中，肝星状细胞的活化最为关键。microRNA（miR）是一类能在转录及转录后水平抑制mRNA表达的短小、单链、非编码RNA，可由细胞外泌体囊泡装载和传递，调节临近和远处的受体细胞的功能。目前已发现许多miR在肝星状细胞活化时的表达发生显著改变，如miR-21、miR-29、miR-708、miR-101、miR-455、miR-146、miR-193等，可通过调节纤维化相关信号通路分子、转录因子等靶基因的表达，调节肝星状细胞的转分化、纤维化发生、增殖、凋亡、自噬等过程，是介导肝纤维化发生和发展的重要物质和表观调节方式。.