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Related Experiment Video

Updated: Feb 23, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
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FXR controls CHOP expression in steatohepatitis.

Claudia D Fuchs1, Thierry Claudel1, Hubert Scharnagl2

  • 1Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Austria.

FEBS Letters
|September 13, 2017
PubMed
Summary

The farnesoid X receptor (FXR) regulates C/EBP homologous protein (CHOP) expression, impacting hepatic lipid metabolism and steatohepatitis. FXR deficiency worsens liver inflammation, highlighting FXR as a key regulator in this disease.

Keywords:
inflammationnonalcoholic fatty liver disease (NAFLD)nonalcoholic steatohepatitis (NASH)nuclear receptor

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Farnesoid X receptor (FXR) and C/EBP homologous protein (CHOP) are crucial for hepatic lipid metabolism.
  • Understanding the interplay between FXR and CHOP is essential for metabolic liver disease research.

Purpose of the Study:

  • To investigate the regulatory relationship between FXR and CHOP in the context of steatohepatitis.
  • To elucidate the molecular mechanisms underlying FXR-mediated regulation of CHOP.

Main Methods:

  • Utilized a methionine- and choline-deficient (MCD) diet model in wild-type (WT) and FXR knockout (KO) mice.
  • Analyzed Chop mRNA expression in liver tissues.
  • Performed experiments in HepG2 cells to confirm FXR/Retinoid X receptor (RXR) dependency.
  • Identified a conserved FXR/RXR-binding site in the human CHOP promoter.

Main Results:

  • Chop mRNA expression was upregulated in WT mice fed the MCD diet but not in FXR KO mice.
  • FXR deficiency exacerbated hepatic inflammation in the MCD diet model.
  • CHOP expression in HepG2 cells was found to be regulated by FXR/RXR.
  • A functional FXR/RXR-binding site was identified in the CHOP promoter, confirming a conserved regulatory pathway.

Conclusions:

  • FXR/RXR signaling directly regulates Chop gene expression.
  • FXR plays a protective role in steatohepatitis by modulating Chop expression and inflammation.
  • This study reveals a novel FXR-CHOP regulatory axis in the pathogenesis of metabolic liver disease.