ReviewGut2022
Novel therapeutic targets for cholestatic and fatty liver disease.
Review in Gut, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.
- Alterations in Circulating Bile Acids in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Systematic Review and Meta-Analysis.Biomolecules · 2023Pooled it
- Gut microbiota-mediated berberine metabolism ameliorates cholestatic liver disease by suppressing 5-hydroxytryptamine production.Clinical and molecular hepatology · 2026Trial
- Comparative effects of aerobic and resistance exercise on bile acid profiles and liver function in patients with non-alcoholic fatty liver disease.BMC gastroenterology · 2025Trial
- The Bile Acid Signaling Axis: Deciphering the Roles of FXR and TGR5 in Hepatic Steatosis, Fibrosis, and Cancer.Pharmacology research & perspectives · 2026Review
- RT206 Couples Partial PPARα/γ Agonism with Ligand-Dependent Allosteric Potentiation of FXR Signaling in Liver Cells.Biomolecules · 2026Article
- Understanding the role of hypoxia inducible factors in liver fibrosis and future therapeutic applications.iLIVER · 2026Review
- Metabolomics and Machine Learning Uncover 5'-Methylthioadenosine as a Metabolic Indicator of Mixed-Pattern Drug-Induced Liver Injury.Metabolites · 2026Article
- Hepatic FXR deficiency exacerbates dyslipidemia by disrupting the gut-liver axis via bile acid disorder and gut microbiota dysbiosis.Journal of translational medicine · 2026Article
- Coregulatory Networks Remodel the Disease-Specific Functions of Orphan Nuclear Receptor TR4.Cells · 2026Review
- Unraveling the HGF/MET axis in Mallory-Denk body pathogenesis associated with liver fibrosis through single-cell transcriptomics.Signal transduction and targeted therapy · 2026Article
- Calculus Bovis ameliorates primary sclerosing cholangitis via a dual-pronged mechanism restoring bile acid and lipid homeostasis in the gut-liver axis.Chinese medicine · 2026Article
- Camelina seeds and their glucosinolate, glucocamelinin, counteract severe fatty liver in rodents with monogenic obesity.Genes & nutrition · 2026Article
- E2F2 transcription factor promotes a cholestatic MASH phenotype by regulating hepatobiliary metabolism through miR-34a-5p.Hepatology (Baltimore, Md.) · 2026Article
- Review
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- Activation of aryl hydrocarbon receptor alleviates cholestatic liver injury by inhibiting inflammation.Cell communication and signaling : CCS · 2026Article
- Article
- Bile acid signaling: from dynamic pool composition to inter-organ communication.Frontiers in endocrinology · 2026Review
- Gut-heart axis at high altitude: a dynamic mediator from hypoxic dysbiosis to adaptive cardioprotection.Frontiers in microbiology · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cholestatic and non-alcoholic fatty liver disease (NAFLD) share several key pathophysiological mechanisms which can be targeted by novel therapeutic concepts that are currently developed for both areas. Nuclear receptors (NRs) are ligand-activated transcriptional regulators of key metabolic processes including hepatic lipid and glucose metabolism, energy expenditure and bile acid (BA) homoeostasis, as well as inflammation, fibrosis and cellular proliferation. Dysregulation of these processes contributes to the pathogenesis and progression of cholestatic as well as fatty liver disease, placing NRs at the forefront of novel therapeutic approaches. This includes BA and fatty acid activated NRs such as farnesoid-X receptor (FXR) and peroxisome proliferator-activated receptors, respectively, for which high affinity therapeutic ligands targeting specific or multiple isoforms have been developed. Moreover, novel liver-specific ligands for thyroid hormone receptor beta 1 complete the spectrum of currently available NR-targeted drugs. Apart from FXR ligands, BA signalling can be targeted by mimetics of FXR-activated fibroblast growth factor 19, modulation of their enterohepatic circulation through uptake inhibitors in hepatocytes and enterocytes, as well as novel BA derivatives undergoing cholehepatic shunting (instead of enterohepatic circulation). Other therapeutic approaches more directly target inflammation and/or fibrosis as critical events of disease progression. Combination strategies synergistically targeting metabolic disturbances, inflammation and fibrosis may be ultimately necessary for successful treatment of these complex and multifactorial disorders.
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What OpenQuestion holds
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.