肝纤维化发生机制的研究进展OA

Hepatic fibrosis is a compensatory response of abnormal repair following hepatocellular injury,induced by long-term exposure to various pathogenic factors such as viral infection,alcoholic injury,and non-alcoholic fatty liver disease.As a core pathological link in the progression of chronic liver diseases,it is characterized by the activation and proliferation of hepatic stellate cells,accompanied by the imbalance of key cytokines including transforming growth factor-β1 and platelet-derived growth factor,as well as the abnormal activation of signaling pathways such as mitogen-activated protein kinase and Smad.Ultimately,this leads to the excessive deposition and degradation imbalance of extracellular matrix components such as collagen and proteoglycans.Uncontrolled progression can result in liver cirrhosis,liver failure,and even hepatocellular carcinoma,making it a major public health concern globally that seriously threatens human health.This article systematically reviews the latest research advances in the cellular mechanisms,cytokine regulation,signaling pathways,and ECM metabolic imbalance involved in the development and progression of hepatic fibrosis in recent years,with a focus on sorting out the crosstalk mechanisms among various regulatory links.The authors propose that the pathological process of hepatic fibrosis is characterized by the complexity of multi-cell involvement and multi-pathway synergistic regulation,and single-target intervention strategies yield limited therapeutic effects.By integrating existing research evidence,this review thoroughly analyzes the core regulatory network of hepatic fibrosis,providing an important theoretical basis for further elucidating the pathogenic mechanisms,developing multi-target combined therapeutic strategies,and identifying novel diagnostic biomarkers.