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Repurposing auranofin in nonalcoholic fatty liver disease still requires further evidence.

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and the of nuclear factor kappa B (NF-κB) and inhibitor of NF-κB alpha (IκBα) in LX-2 cells; in HepG2 auranofin erythroid 2-related factor 2 (NRF2) significantly and was required for… Click to show full abstract

and the of nuclear factor kappa B (NF-κB) and inhibitor of NF-κB alpha (IκBα) in LX-2 cells; in HepG2 auranofin erythroid 2-related factor 2 (NRF2) significantly and was required for auranofin to exhibit insulin sensitizing effects. The presence of hyperleptinemia and leptin resistance in obese patients suggests that partial reduction of leptin by auranofin may be used as a strategy against obesity and NAFLD. The interferon regulatory factor 3 (IRF3) signaling pathway promotes hepatocyte inflammation and apoptosis in NAFLD. Auranofin inhibited fatty acid-induced hepatocyte apoptosis in an in vitro model by inducing cellular autophagy and thereby degrading IRF3.

Keywords: nonalcoholic fatty; fatty liver; auranofin nonalcoholic; disease still; repurposing auranofin; liver disease

Journal Title: Clinical and molecular hepatology
Year Published: 2022

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