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Hepatic stellate cell (HSC) proliferation refers to the process by which these liver-resident pericytes increase in number, particularly in response to liver injury or chronic inflammation. HSCs are normally quiescent but become activated and proliferative during liver damage, playing a central role in fibrogenesis and the pathogenesis of cirrhosis and hepatocellular carcinoma (HCC). Key pathways involved include glutamine metabolism and growth factor/cytokine signaling. Targeting these pathways represents promising strategies against liver fibrosis.
Inhibition of metabolic enzymes (e.g., glutaminase) or growth factor signaling pathways (e.g., PDGF, TGF-β) to reduce HSC proliferation and ECM production.
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