ReviewBritish journal of pharmacology2009
Nuclear receptors as therapeutic targets in cholestatic liver diseases.
Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 139 citations in OpenAlex.
- Cynaroside Attenuates Ethinylestradiol-Induced Cholestatic Liver Injury by Modulating the FXR/BSEP/CYP7A1/SHP Axis.International journal of molecular sciences · 2026Article
- Oxidative Stress in Biotoxin-Induced Liver Injury: From ROS Generation to Cell Death and Therapeutic Intervention.Toxics · 2026Review
- Phenobarbital Treatment for Prolonged Cholestatic Jaundice After Endoscopic Retrograde Cholangiopancreatography.ACG case reports journal · 2026Article
- Development of novel liver-targeting glucocorticoid prodrugs.Medicine in drug discovery · 2024Article
- Recent Advances in Hepatic Metabolic Regulation by the Nuclear Factor Rev-erbɑ.Current drug metabolism · 2024Review
- Unraveling the mechanisms underlying drug-induced cholestatic liver injury: identifying key genes using machine learning techniques on human in vitro data sets.Archives of toxicology · 2023Article
- Current Therapeutics in Primary Sclerosing Cholangitis.Journal of clinical and translational hepatology · 2023Review
- Narrative Review: Glucocorticoids in Alcoholic Hepatitis-Benefits, Side Effects, and Mechanisms.Journal of xenobiotics · 2022Review
- Serum 25-hydroxyvitamin D and C-reactive protein and plasma von Willebrand concentrations in 23 dogs with chronic hepatopathies.Journal of veterinary internal medicine · 2022Article
- Novel Bile Acid-Dependent Mechanisms of Hepatotoxicity Associated with Tyrosine Kinase Inhibitors.The Journal of pharmacology and experimental therapeutics · 2022Article
- Role of YAP1 Signaling in Biliary Development, Repair, and Disease.Seminars in liver disease · 2022Review
- The Impact of Aging on the Lung Alveolar Environment, Predetermining Susceptibility to Respiratory Infections.Frontiers in aging · 2022Review
- Review
- Bile acid-based therapies for non-alcoholic steatohepatitis and alcoholic liver disease.Hepatobiliary surgery and nutrition · 2020Review
- Emodin Rescues Intrahepatic Cholestasis via Stimulating FXR/BSEP Pathway in Promoting the Canalicular Export of Accumulated Bile.Frontiers in pharmacology · 2019Article
- Mechanistic insights into geniposide regulation of bile salt export pump (BSEP) expression.RSC advances · 2018Article
- Altered Expression of Retinol Metabolism-Related Genes in an ANIT-Induced Cholestasis Rat Model.International journal of molecular sciences · 2018Article
- Effects of corilagin on alleviating cholestasis via farnesoid X receptor-associated pathways in vitro and in vivo.British journal of pharmacology · 2018Article
- Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2018Review
- Targeting H19, an Imprinted Long Non-Coding RNA, in Hepatic Functions and Liver Diseases.Diseases (Basel, Switzerland) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.