Cited by 146Drug Transport and Resistance MechanismsCholesterol and Lipid MetabolismLiver Diseases and Immunity

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Nuclear receptors as therapeutic targets in cholestatic liver diseases

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Zollner, Gernot, Trauner, Michael·2009·British Journal of Pharmacology

DOI 10.1111/j.1476-5381.2008.00030.xPMC PMC2697779

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Abstract

Cholestasis results in intrahepatic accumulation of cytotoxic bile acids, which cause liver damage ultimately leading to biliary fibrosis and cirrhosis. Cholestatic liver injury is counteracted by a variety of adaptive hepatoprotective mechanisms including alterations in bile acid transport, synthesis and detoxification. The underlying molecular mechanisms are mediated mainly at a transcriptional level via a complex network involving nuclear receptors including the farnesoid X receptor, pregnane X receptor, vitamin D receptor and constitutive androstane receptor, which target overlapping, although not identical, sets of genes. Because the intrinsic adaptive response to bile acids cannot fully prevent liver injury in cholestasis, therapeutic targeting of these receptors via specific and potent agonists may further enhance the hepatic defence against toxic bile acids. Activation of these receptors results in repression of bile acid synthesis, induction of phases I and II bile acid hydroxylation and conjugation and stimulation of alternative bile acid export while limiting hepatocellular bile acid import. Furthermore, the use of nuclear receptor ligands may not only influence bile acid transport and metabolism but may also directly target hepatic fibrogenesis and inflammation. Many drugs already used to treat cholestasis and its complications such as pruritus (e.g. ursodeoxycholic acid, rifampicin, fibrates) may act via activation of nuclear receptors. More specific and potent nuclear receptor ligands are currently being developed. This article will review the current knowledge on nuclear receptors and their potential role in the treatment of cholestatic liver diseases.

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Authors: Zollner, G., & Trauner, M.
Affiliations: Medical University of Graz (AT)
Corresponding author: Trauner, Michael
ORCID: Zollner, Gernot
Trauner, Michael
Venue: British Journal of Pharmacology
Publisher: Wiley
Published: 2008-12-24
Volume: 156
Issue: 1
Pages: 7-27
ISSN: 0007-1188 (ISSN-L)
1476-5381
DOI: 10.1111/j.1476-5381.2008.00030.x
PMC: PMC2697779
OpenAlex: W2022838513
Cited by: 146
References: 304
Citations by year: 2026: 6 · 2025: 2 · 2024: 6 · 2023: 4 · 2022: 11 · 2021: 4 · 2020: 7 · 2019: 7 · 2018: 6 · 2017: 6 · 2016: 11 · 2015: 7 · 2014: 14 · 2013: 12 · 2012: 9
FWCI: 1.09
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: British Journal of Pharmacology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Keywords: nuclear receptors, cholestasis, cholestatic liver injury, farnesoid X receptor, pregnane X receptor, vitamin D receptor, constitutive androstane receptor, bile acid metabolism, bile acid transport, bile acid detoxification, hepatoprotection, liver fibrosis, liver cirrhosis, nuclear receptor agonists, ursodeoxycholic acid, pruritus, liver inflammation
MeSH terms: Bile Acids and Salts, Cholestasis, Chronic Disease, Humans, Ligands, Liver, Liver Cirrhosis, Receptors, Cytoplasmic and Nuclear

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Nuclear receptors as therapeutic targets in cholestatic liver diseases

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