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Hepatic stellate cell (HSC) activation refers to the process by which quiescent, vitamin A-storing HSCs in the liver transdifferentiate into proliferative, contractile, and fibrogenic myofibroblast-like cells. This transition is a central event in liver fibrosis and occurs in response to chronic liver injury from various causes such as viral hepatitis, alcohol abuse, or non-alcoholic steatohepatitis (NASH). Persistent hepatic stellate cell activation underlies progressive liver fibrosis—a precursor for cirrhosis and hepatocellular carcinoma if unresolved. Antifibrotic strategies target various aspects of the process: Inhibiting proliferation/survival signals for activated HSCs, Promoting apoptosis/senescence/reversion toward inactivity, Blocking key profibrotic mediators. Emerging therapies also focus on metabolic modulation or epigenetic reprogramming as means to halt/reverse fibrogenesis driven by activated stellate cells.
Inhibition of proliferation/survival signals, promotion of apoptosis/senescence/reversion toward inactivity, blocking profibrotic mediators, metabolic modulation, epigenetic reprogramming
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