Nuclear Receptors in Liver Disease Δ
Open accessAbstract
Nuclear receptors are ligand-activated transcriptional regulators of several key aspects of hepatic physiology and pathophysiology. As such, nuclear receptors control a large variety of metabolic processes including hepatic lipid metabolism, drug disposition, bile acid homeostasis, as well as liver regeneration, inflammation, fibrosis, cell differentiation, and tumor formation. Derangements of nuclear receptor regulation and genetic variants may contribute to the pathogenesis and progression of liver diseases. This places nuclear receptors into the frontline for novel therapeutic approaches for a broad range of hepatic disorders and diseases including cholestatic and fatty liver disease, drug hepatotoxicity, viral hepatitis, liver fibrosis, and cancer. (Hepatology 2011;.)
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RXR usually forms heterodimers with several other NRs such as FXR, PPAR and LXR, and thereby has broad implications for fibrogenesis.
“The retinoid X receptor (RXR) usually forms heterodimers with several other NRs (e.g., FXR, PPAR, LXR) and thereby has broad implications for fibrogenesis.[169]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [169]
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- Authors
- Wagner, M., Zollner, G., & Trauner, M.
- Affiliations
- Baylor College of Medicine (US)
- Medical University of Graz (AT)
- Medical University of Vienna (AT)
- Corresponding author
- Trauner, Michael
- Venue
- Hepatology
- Published
- 2011-03
- Volume
- 53
- Issue
- 3
- Pages
- 1023-1034
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W1966064283
- Cited by
- 260
- References
- 7
- Citations by year
- 2026: 3 · 2025: 14 · 2024: 8 · 2023: 4 · 2022: 17 · 2021: 23 · 2020: 12 · 2019: 17 · 2018: 17 · 2017: 21 · 2016: 21 · 2015: 22 · 2014: 24 · 2013: 29 · 2012: 19
- FWCI
- 16.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion)
- Funders
- Austrian Science Foundation and funding from the European Community's Seventh Framework Programme (P18613-B05, F3008-B05)
- FLIP (FP7/2007-2013, HEALTH-F2-2009-241762)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- nuclear receptors, liver disease, hepatic lipid metabolism, bile acid homeostasis, drug disposition, liver regeneration, liver fibrosis, liver inflammation, hepatic steatosis, cholestatic liver disease, drug-induced liver injury, viral hepatitis, liver cancer, transcriptional regulation
- MeSH terms
- Bile Acids and Salts, Cholestasis, Fatty Liver, Glucose, Hepatitis, Hepatitis B, Hepatitis C, Carcinoma, Hepatocellular, Humans, Cholesterol, HDL, Liver, Liver Cirrhosis, Liver Diseases, Liver Regeneration, Transcription, Genetic, Triglycerides, Receptors, Cytoplasmic and Nuclear, Lipid Metabolism, Chemical and Drug Induced Liver Injury, Non-alcoholic Fatty Liver Disease
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