Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.5, p. 349–361, 2025

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
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General Physiology and Biophysics Vol.44, No.5, p. 349–361, 2025

Title: HuR enhances the stability of FGF19 mRNA to suppress Kupffer cell activation and mitigate inflammation and fibrosis in non-alcoholic fatty liver disease
Author: XiaoQing Mo, SiJun Zhou, XiaoGe Zhou, Chun Huang
Abstract: This study explores how human antigen R (HuR) stabilizes fibroblast growth factor 19 (FGF19) mRNA, inhibiting Kupffer cell (KC) activation to reduce inflammation and fibrosis in non-alcoholic fatty liver disease (NAFLD). An animal model of NAFLD was established in mice by administering a high-fat diet (HFD). In vitro study utilized a lipopolysaccharide-induced immortalized mouse KC model. HuR expression markedly decreased in HFD-induced NAFLD liver tissue. Overexpression of HuR via adeno-associated virus (AAV) vectors mitigated key pathological features of NAFLD, including hepatic inflammation and fibrosis. Moreover, HuR overexpression suppressed KC activation in both in vitro and in vivo models. Mechanistically, HuR bound AU-rich elements in FGF19 mRNA, enhancing its stability. FGF19 overexpression similarly mitigated HFD-induced liver pathology. Conversely, FGF19 silencing reversed HuR's inhibition of KC activation and abrogated HuR's protection against liver inflammation and fibrosis. This research elucidates a novel mechanism underlying the interaction between HuR and FGF19 in mitigating the pathological progression of NAFLD, providing potential therapeutic targets for this prevalent liver disease.
Keywords: HuR — NAFLD — Kupffer cells — FGF19 — Inflammation — Fibrosis
Year: 2025, Volume: 44, Issue: 5 Page From: 349, Page To: 361
doi:10.4149/gpb_2025023


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