ArticleHepatology international2026
FXR overexpression promotes liver regeneration through inducing FGF2 activation in APAP-induced acute liver injury.
Article in Hepatology international, 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
background and purposeAcetaminophen (APAP)-induced hepatotoxicity represents a critical medical emergency due to the rapid progression. To date, practical and feasible early interventions are limited. This study aimed to explore whether farnesoid X receptor (FXR, NR1H4) alleviates APAP-induced acute liver injury and whether this effect is mediated by fibroblast growth factor 2 (FGF2) activation to promote liver regeneration.
methodsThe difference in FXR expression between healthy subjects and patients with APAP-induced acute liver injury was analyzed through the Gene Expression Omnibus (GEO) database. The adeno-associated virus-8-mediated FXR (AAV-FXR) was injected through the tail vein into mice to establish the mouse FXR-overexpressed model. pcDNA-FXR, siFXR or siFGF2 plasmids were transfected into AML-12 cells. H&E staining, quantitative real-time PCR, Western blotting, immunofluorescence staining, DCFH-DA staining, and TUNEL staining were applied to determine the effects of FXR and FGF2.
resultsFXR was significantly reduced in hepatic tissues of patients with APAP-induced acute liver injury compared to normal hepatic tissues. FXR overexpression attenuated APAP-induced liver injury by inhibiting inflammation, oxidative stress and apoptosis, while promoting liver regeneration. Furthermore, FXR overexpression upregulated FGF2 expression, and its pro-regenerative effect against APAP-induced acute liver injury is dependent on FGF2. In contrast, FXR or FGF2 knockdown resulted in opposite effects.
conclusionsFXR alleviated APAP-induced acute liver injury by mitigating inflammation, oxidative stress and apoptosis, as well as promoting liver regeneration. This pro-regenerative effect of FXR is dependent on FGF2 activation.
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