FIGURE 1.

Schematic diagram of the central role of HSCs in the fibrogenesis and regression of liver fibrosis. Upon various chronic liver injuries, the hepatocytes and biliary epithelial cells can be damaged, together with Kupffer cells and macrophages, release chemokines, and cytokines to activate the HSCs. aHSCs are prone to present characteristics including retinoid loss, proliferation, contractility, ECM production, altered matrix degradation, chemotaxis, and expressing inflammatory signals. Liver fibrosis may develop into cirrhosis and even liver cancer, along with a suite of complications, such as portal hypertension, hepatic encephalopathy, and liver failure. Currently, the main antifibrotic therapy strategies are inhibiting HSC activation and proliferation, reversing the activation phenotype to the quiescent phenotype, or inducing HSC apoptosis and senescence. Abbreviations: qHSC, quiescent hepatic stellate cell; aHSCs, activated hepatic stellate cell.