ArticleGastroenterology2019
Aryl Hydrocarbon Receptor Signaling Prevents Activation of Hepatic Stellate Cells and Liver Fibrogenesis in Mice.
Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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Who cites it
58 citing papers in PubMed, 104 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Gut microbiota-driven indole-3-propionic acid and kynurenine production is associated with improved metabolic adaptation in periparturient dairy cows.Journal of animal science and biotechnology · 2026Article
- Article
- Review
- Asiaticoside protects against PDF-induced peritoneal fibrosis via suppression of AhR/Nrf2-mediated MMT and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Activation of aryl hydrocarbon receptor alleviates cholestatic liver injury by inhibiting inflammation.Cell communication and signaling : CCS · 2026Article
- Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD.EBioMedicine · 2026Article
- The role of tryptophan-AhR signaling in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD): implications for therapeutic strategies.Frontiers in immunology · 2026Review
- Aryl hydrocarbon receptor: a multifaceted environmental sensor in liver homeostasis and disease.Frontiers in medicine · 2026Review
- AHR Deficiency Exacerbates Hepatic Cholesterol Accumulation via Inhibiting Bile Acid Synthesis in MAFLD Rats.International journal of molecular sciences · 2025Article
- Liver fibrosis with persistently normal alanine transaminase levels exhibits a distinct treatment response in MASLD.BMJ open gastroenterology · 2025Article
- Macrophage-Mediated Transport of Insoluble Indirubin Induces Hepatic Injury During Intestinal Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Microbiota-derived indole acetic acid extends lifespan through the AhR-Sirt2 pathway inmSystems · 2025Article
- The AhR/IL-22 axis in chronic gut inflammation: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- The aryl hydrocarbon receptor in liver injury: a double-edged sword in roles, mechanisms, and future perspectives.Frontiers in pharmacology · 2025Review
- Bone Marrow Mesenchymal Stem Cells Can Prevent Pancreatic Fibrosis in Mice with Chronic Pancreatitis by Inhibiting the Activation of Pancreatic Stellate Cells.Journal of inflammation research · 2025Article
- Aryl Hydrocarbon Receptor Alleviates Hepatic Fibrosis by Inducing Hepatic Stellate Cell Ferroptosis.Journal of cellular and molecular medicine · 2024Article
- Inhibition of heme-thiolate monooxygenase CYP1B1 prevents hepatic stellate cell activation and liver fibrosis by accumulating trehalose.Science translational medicine · 2024Article
- Article
- Commensal microbe regulation of skin cells in disease.Cell host & microbe · 2024Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsThe role of aryl hydrocarbon receptor (AhR) in liver fibrosis is controversial because loss and gain of AhR activity both lead to liver fibrosis. The goal of this study was to investigate how the expression of AhR by different liver cell types, hepatic stellate cells (HSCs) in particular, affects liver fibrosis in mice.
methodsWe studied the effects of AhR on primary mouse and human HSCs, measuring their activation and stimulation of fibrogenesis using RNA-sequencing analysis. C57BL/6J mice were given the AhR agonists 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE); were given carbon tetrachloride (CCl
resultsAhR was expressed at high levels in quiescent HSCs, but the expression decreased with HSC activation. Activation of HSCs from AhR-knockout mice was accelerated compared with HSCs from wild-type mice. In contrast, TCDD or ITE inhibited spontaneous and transforming growth factor β-induced activation of HSCs. Mice with disruption of Ahr in HSCs, but not hepatocytes or Kupffer cells, developed more severe fibrosis after administration of CCl
conclusionsIn studies of human and mouse HSCs, we found that AhR prevents HSC activation and expression of genes required for liver fibrogenesis. Development of nontoxic AhR agonists or strategies to activate AhR signaling in HSCs might be developed to prevent or treat liver fibrosis.
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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 Socratic graph.