[Interactions between transforming growth factor beta and signal transducer and activator of transcription 3 in the development of liver fibrosis].

Liver fibrosis is a common pathological response in chronic liver injury. In the pathological process of hepatic injury, signaling pathways associated with hepatic fibrosis, which mediates the repair, proliferation and fibrosis of the liver secrete different cytokines. In these pathways, transforming growth factor beta (TGFβ) and signal transducer and activator of transcription 3 (STAT3) play key roles in the proliferation and activation of hepatic stellate cells (HSCs) and promote epithelial mesenchymal transition. In addition, it is also involved in the process of proliferation and transformation of collagen and extracellular matrix molecules into myofibroblasts. TGFβ and STAT3 molecular-related signaling pathways mediate the loss of epithelial phenotype and gene expression in mature epithelial cells, transforming them into mesenchymal cells, and producing anti-apoptosis to hepatocytes and promoting the proliferation of HSCs. However, the mechanisms by which STAT3 and TGFβ molecules are involved in the development and progression of liver fibrosis are not sound distinct. In this review, we attempt to know the mechanisms and interactions of TGFβ and STAT3 molecules that mediate potential liver fibrosis, and promote their role in promoting HSCs production and epithelial mesenchymal transition.肝纤维化是慢性肝损伤中常见的病理反应。在肝损伤的病理过程中，不同细胞因子通过与肝纤维化有关的信号传导途径分泌，介导肝细胞的修复、增生以及肝脏的纤维化。在这些途径中，转化生长因子β（TGFβ）和信号转导和转录激活因子3（STAT3）在肝星状细胞（HSCs）的增殖和活化中起关键作用，并促进上皮间充质转化反应发生，这在肝纤维化过程中起到了至关重要的作用，其中还包含胶原和细胞外基质分子增生以及向肌成纤维细胞转化。TGFβ和STAT3分子相关信号通路介导成熟上皮细胞失去上皮表型和基因表达，使其转变为间充质细胞，并有对肝细胞产生抗凋亡和促进HSCs增殖作用。然而，STAT3和TGFβ分子对肝纤维化发生和进展相关机制尚未明确。拟通过综述了解有关TGFβ和STAT3分子介导潜在的肝纤维化机制，并探讨它们在促进HSCs生成和上皮间充质转化反应过程中的关系和相互作用。.