Fig. 7 |. Key pathways of liver fibrosis progression and regression.

a, Injury to hepatocytes results in the release of damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) that activate resident and infiltrating immune cells in the liver and hepatic stellate cells (HSCs). In turn, pro-inflammatory cytokines and chemokines and profibrogenic cytokines are released that further stimulate the differentiation, migration and activity of HSCs. b, Regression of fibrosis occurs if the damaging insults are removed. Then, the hepatocytes can proliferate to replace injured hepatocytes, and HSCs are inactivated via reversion to a quiescent phenotype, cell death or cellular senescence. In murine models, extracellular matrix degradation is promoted by the activity of pro-resolution Ly6C^lo monocytes and the activity of matrix metalloproteinases. MASLD, metabolic dysfunction-associated steatotic liver disease; PDGF, platelet-derived growth factor; TGFβ, transforming growth factor-β.