Table 1.
STAT Proteins | Major Triggers or Cytokines | Possible Roles in Fibrotic Liver |
---|---|---|
STAT1 | IFN-α, IFN-β, IFN-γ | Hepatic Stellate Cells→Loss→Inhibited proliferation, increased apoptosis and blocked cell cycle Hepatocytes→Inhibition of liver regeneration, and pro-apoptosis |
STAT2 | IFN-α, IFN-β, IFN-λ | Promote antiviral responses Protect against hepatic fibrosis |
STAT3 | IL-6, IL-22 | Hepatocytes→Loss→Increased inflammation in the CCl4-induced chronic model Hepatocytes→Loss→Reduced inflammation in the CCl4-induced acute model |
STAT4 | IL-12, IFN-γ | Impaired STAT4 phosphorylation→liver inflammation and fibrosis Promotes liver inflammation |
STAT5 | GH, IL-2, IL-3, IL-5 | Hepatocytes→Loss→Increased TGF-β levels, increased the sensitivity of Kupffer or hepatic stellate cells to TGF-β Hepatocytes→Loss→Reduces proliferation Antifibrotic effects in the mouse model of cholestasis |
STAT6 | IL-4, IL-13 | Hepatocytes→Loss→Reduced collagen deposition Hepatic Stellate Cells→Promotes liver fibrogenesis Promotes inflammation in hepatitis Protects against ischemia/reperfusion and inflammation of drug-induced liver injuries |
References are cited in the text.