ArticleThe American journal of pathology2018
The Secretin/Secretin Receptor Axis Modulates Ductular Reaction and Liver Fibrosis through Changes in Transforming Growth Factor-β1-Mediated Biliary Senescence.
Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Advances in pharmacological interventions for hepatic fibrosis: from pathogenic mechanisms to novel therapeutic targets.Annals of medicine · 2026Review
- Mesenchymal stem cell-derived extracellular vesicles attenuate periductal fibrosis by inhibiting Th17 differentiation in human liver multilineage organoids and Mdr2Journal of nanobiotechnology · 2025Article
- Portal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities.Gastroenterology · 2025Review
- MSC-derived exosomes attenuate hepatic fibrosis in primary sclerosing cholangitis through inhibition of Th17 differentiation.Asian journal of pharmaceutical sciences · 2024Article
- Sequence of events leading to primary biliary cholangitis.World journal of gastroenterology · 2023Review
- Knockout of secretin ameliorates biliary and liver phenotypes during alcohol-induced hepatotoxicity.Cell & bioscience · 2023Article
- Pathophysiological Roles of Ductular Reaction in Liver Inflammation and Hepatic Fibrogenesis.Cellular and molecular gastroenterology and hepatology · 2023Article
- Review
- Liver secretin receptor predicts portoenterostomy outcomes and liver injury in biliary atresia.Scientific reports · 2022Article
- Recent discoveries in microbiota dysbiosis, cholangiocytic factors, and models for studying the pathogenesis of primary sclerosing cholangitis.Open medicine (Warsaw, Poland) · 2022Review
- Inhibition of Secretin/Secretin Receptor Axis Ameliorates NAFLD Phenotypes.Hepatology (Baltimore, Md.) · 2021Article
- Organoids and Spheroids as Models for Studying Cholestatic Liver Injury and Cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2021Review
- Mast Cells Induce Ductular Reaction Mimicking Liver Injury in Mice Through Mast Cell-Derived Transforming Growth Factor Beta 1 Signaling.Hepatology (Baltimore, Md.) · 2021Article
- Biliary Epithelial Senescence in Liver Disease: There Will Be SASP.Frontiers in molecular biosciences · 2021Review
- The Dynamic Interplay Between Mast Cells, Aging/Cellular Senescence, and Liver Disease.Gene expression · 2020Review
- Biliary damage and liver fibrosis are ameliorated in a novel mouse model lacking l-histidine decarboxylase/histamine signaling.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Melatonin and circadian rhythms in liver diseases: Functional roles and potential therapies.Journal of pineal research · 2020Review
- Cholangiocarcinoma: novel therapeutic targets.Expert opinion on therapeutic targets · 2020Review
- Review
- The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis.Hepatology (Baltimore, Md.) · 2020Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Activation of the secretin (Sct)/secretin receptor (SR) axis stimulates ductular reaction and liver fibrosis, which are hallmarks of cholangiopathies. Our aim was to define the role of Sct-regulated cellular senescence, and we demonstrated that both ductular reaction and liver fibrosis are significantly reduced in Sct
Indexed as
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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.