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Hepatic stellate cell activation inhibition refers to the therapeutic strategy of preventing or reversing the activation of hepatic stellate cells (HSCs) from a quiescent to a myofibroblast-like, fibrogenic state. Activated HSCs drive the progression of liver fibrosis by proliferating, migrating, and excessively depositing extracellular matrix proteins in response to liver injury. Inhibition of this activation can be achieved via small molecules, biologics, or gene modulators that interfere with specific signaling pathways (e.g., TGF-β, hedgehog, Wnt), profibrotic cytokines, metabolic processes, or epigenetic regulators. This process is a central target in antifibrotic therapy, but it does not correspond to a single, specific molecular target[5][3][7][8].
Induction of HSC apoptosis; Inhibition of HSC proliferation; Inhibition of TGF-β signaling; Blockade of hedgehog, Wnt, and other profibrotic pathways; Epigenetic modulation (e.g., DNMT3B inhibition); Autophagy modulation; Modulation of cytokine/receptor pathways (e.g., using targeted delivery via cytokine receptors).
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