ArticleStem cell research & therapy2026
HMGB1-mediated enhancement of glycolysis activates hepatic stellate cells by inhibiting ferroptosis in alcoholic hepatic fibrosis.
Article in Stem cell research & therapy, 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
backgroundAlcoholic hepatic fibrosis (AHF) ultimately leads to liver cirrhosis and even hepatocellular carcinoma. The aim of this study was to investigate the specific mechanism by which high mobility group protein B1 (HMGB1) regulated the activation of hepatic stellate cells (HSCs) in AHF.
methodsCCK-8, EdU staining and flow cytometry assays were utilized to evaluate the viability, proliferation and apoptosis of LX-2 cells stimulated by ethanol. The effect of HMGB1 on cell glycolysis was assessed by cellular energy metabolism assays. The levels of Fe
resultsEthanol stimulation significantly upregulated HMGB1 and HSC activation markers, enhanced glycolysis, and inhibited ferroptosis in LX-2 cells. Knockdown of HMGB1 suppressed ethanol-induced effects, including HSC activation and glycolysis promotion. However, these effects of HMGB1 knockdown were negated by an oxidative phosphorylation inhibitor. Furthermore, a ferroptosis inducer impeded ethanol-induced HSC activation. Overexpression of HMGB1 decreased the ferroptosis level in ethanol-stimulated LX-2 cells, which was reversed by a glycolysis inhibitor. These in vitro findings demonstrated that upregulated HMGB1 inhibited ferroptosis by enhancing glycolysis, thereby promoting HSC activation. In vivo validation data further confirmed that HMGB1 knockdown inhibited glycolysis, increased ferroptosis level, reduced HSC activation, and alleviated liver fibrosis in AHF mice. Ferroptosis inhibitor counteracted the impacts of HMGB1 knockdown on ferroptosis, HSC activation and liver fibrosis in AHF mice.
conclusionIn summary, HMGB1 promoted the metabolism of HSCs towards glycolysis to inhibit ferroptosis, which eventually led to the activation of HSCs and the progression of AHF.
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