ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Nuclear Factor I-B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a significant contributor to liver fibrosis due to hepatic stellate cells (HSCs) activation. The anti-apoptotic gene Nuclear Factor I-B (NFIB) has been implicated in regulating cell proliferation and differentiation in the context of liver injury. However, its role in HSCs differentiation remains unclear. Our study reveals NFIB as the most markedly down-regulated transcription factor during HSCs activation, as evidenced by single-cell sequencing analysis of liver fibrosis. Clinical examination of liver tissues from MASH fibrosis patients corroborated diminished NFIB expression in HSCs across varying fibrosis stages. Using a murine model of liver fibrosis induced by a choline-deficient, amino acid-restricted high-fat diet (CDAHFD) and carbon tetrachloride (CCl
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