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Targeting FXR in Cholestasis.

Verena Keitel1, Carola Dröge2, Dieter Häussinger2

  • 1Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty at Heinrich-Heine-University, Düsseldorf, Germany. Verena.Keitel@med.uni-duesseldorf.de.

Handbook of Experimental Pharmacology
|June 16, 2019
PubMed
Summary
This summary is machine-generated.

The farnesoid X receptor (FXR) is crucial for bile acid (BA) balance. Genetic defects in FXR cause severe early-onset cholestasis in children, highlighting its vital role in liver health and BA regulation.

Keywords:
Bile acid homeostasisCholestasisFGF19Farnesoid X receptor (FXR)Fibroblast growth factorObeticholic acidPrimary biliary cholangitis (PBC)Primary sclerosing cholangitis (PSC)

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Area of Science:

  • Hepatology and Gastroenterology
  • Molecular Endocrinology
  • Genetics and Disease

Background:

  • The farnesoid X receptor (FXR) is a bile acid-activated transcription factor vital for maintaining bile acid (BA) homeostasis.
  • FXR regulates key genes involved in BA synthesis, detoxification, secretion, and absorption within the enterohepatic circulation.
  • FXR also influences lipid and glucose metabolism and inflammatory responses.

Purpose of the Study:

  • To summarize the current understanding of FXR's role in cholestasis, encompassing both rodent models and human diseases.
  • To highlight the clinical significance of FXR defects in severe, early-onset cholestatic liver conditions.

Main Methods:

  • Review of scientific literature on FXR function in cholestasis.
  • Analysis of genetic studies identifying FXR variants in human cholestatic diseases.
  • Examination of data from rodent models of cholestasis involving FXR manipulation.

Main Results:

  • Targeted deletion of FXR in mice leads to increased susceptibility to cholestatic liver injury.
  • Combined deletion of FXR and SHP in mice triggers early-onset progressive familial intrahepatic cholestasis (PFIC).
  • Homozygous FXR variants in humans cause severe, early-onset PFIC and liver failure.

Conclusions:

  • FXR plays a central role in regulating systemic and hepatic BA levels.
  • Dysfunctional FXR is implicated in human cholestatic conditions like PFIC and intrahepatic cholestasis of pregnancy.
  • Targeting FXR with agonists or FGF19 analogues represents a therapeutic strategy for cholestatic liver diseases.