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Nuclear Factor I-B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription

Qianqian Chen1,2,3,4, Fajuan Rui1,2,3, Zhiwen Fan5

  • 1Department of Infectious Diseases, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|December 23, 2025
PubMed

Insights

Nuclear Factor I-B (NFIB) is downregulated in liver fibrosis. Restoring NFIB suppresses chemokine CCL5, reduces oxidative stress, and mitigates liver fibrosis, offering a new therapeutic target.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Fibrosis Research

Background:

  • Metabolic dysfunction-associated steatohepatitis (MASH) drives liver fibrosis via hepatic stellate cell (HSC) activation.
  • Nuclear Factor I-B (NFIB) is an anti-apoptotic gene involved in cell regulation, but its role in HSC differentiation is unknown.

Purpose of the Study:

  • Investigate the role of NFIB in HSC activation and liver fibrosis.
  • Elucidate the mechanism of NFIB action in liver fibrosis progression.

Main Methods:

  • Single-cell sequencing of liver fibrosis to identify transcription factor changes.
  • Analysis of human MASH fibrosis patient liver tissues.
  • Murine models of liver fibrosis (CDAHFD and CCl4).
  • NFIB overexpression studies and RNA sequencing.

Main Results:

  • NFIB is significantly downregulated during HSC activation and in MASH fibrosis patients.
  • NFIB overexpression reduces liver fibrosis in murine models.
  • NFIB directly suppresses chemokine CCL5 expression by interacting with its promoter.
  • NFIB mitigates liver fibrosis by inhibiting oxidative stress.

Conclusions:

  • NFIB plays a critical role in regulating HSC activation and liver fibrosis.
  • The NFIB/CCL5 axis is a novel mechanism in liver fibrosis progression.
  • Targeting the NFIB/CCL5 pathway presents a potential therapeutic strategy for liver fibrosis.
Keywords:
Chemokine C─C motif ligand 5hepatic stellate cellsliver fibrosismetabolic dysfunction‐associated steatohepatitisnuclear factor I‐B

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