Abstract:

Hepatic fibrosis （HF） is a common pathological repair response occurring after liver injury and is a critical stage in the progression of chronic liver diseases towards cirrhosis. The molecular mechanisms of HF occurrence are complex. Liver injury triggers the release of various cytokines by multiple cell types， and initiates the downstream signaling pathways to activate the hepatic stellate cells （HSCs） and transform them into myofibroblasts （MFBs）. MFBs can release large quantities of extracellular matrix （ECM）， thereby disrupt the normal liver architecture and lead to the occurrence and development of HF. The potential therapeutic targets for HF are still in the experimental animal phase， and there are no clinical applications yet. This review summarizes the signaling pathways and related factors involving HSCs and ECM in HF， such as the transforming growth factor-β （TGF-β）/Smad signaling pathway， platelet-derived growth factor （PDGF）， matrix metalloproteinases （MMPs）， tissue inhibitors of metalloproteinases （TIMPs）， and connective tissue growth factor （CTGF）. It also discusses the related therapeutic targets， and provids the theoretical basis for the development of new drugs for HF.

Key words: Hepatic fibrosis, Hepatic stellate cell, Extracellular matrix, Molecular mechanism, Therapeutic target