ArticlePloS one2022
Periductal bile acid exposure causes cholangiocyte injury and fibrosis.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Reply to: "Enhancing biliary protection via HOPE: Beyond bile composition to cholangiocyte resilience".JHEP reports : innovation in hepatology · 2026Article
- Macrophage signaling associates with fibrogenic program activation in periductal fibroblasts in pediatric primary sclerosing cholangitis.JCI insight · 2026Article
- Pediatric Cholestatic Diseases in the Era of Ileal Bile Acid Transporter (IBAT) Inhibitors.Pediatric reports · 2026Review
- The bile acid-gut microbiota-vitamin D axis: new insights into biliary atresia.Frontiers in cellular and infection microbiology · 2026Review
- Biliary atresia.Nature reviews. Disease primers · 2024Review
- Comprehensive bile acid pool analysis during ex-vivo liver perfusion in a porcine model of ischemia-reperfusion injury.Scientific reports · 2024Article
- Article
- Biliatresone induces cholangiopathy in C57BL/6J neonates.Scientific reports · 2023Article
- In Utero Extrahepatic Bile Duct Damage and Repair: Implications for Biliary Atresia.Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology SocietyReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionBile duct integrity is essential for the maintenance of the structure and function of the biliary tree. We previously showed that cholangiocyte injury in a toxic model of biliary atresia leads to increased monolayer permeability. Increased epithelial permeability was also shown in other cholangiopathies. We hypothesized that after initial cholangiocyte injury, leakage of bile acids into the duct submucosa propagates cholangiocyte damage and fibrosis. We thus aimed to determine the impact of bile acid exposure on cholangiocytes and the potential therapeutic effect of a non-toxic bile acid. MATERIALS AND
methodsExtrahepatic bile duct explants were isolated from adult and neonatal BALB/c mice. Explants were cultured with or without glycochenodeoxycholic acid and ursodeoxycholic acid. They were then fixed and stained.
resultsExplants treated with glycochenodeoxycholic acid demonstrated cholangiocyte injury with monolayer disruption and partial lumen obstruction compared to control ducts. Masson's trichrome stains revealed increased collagen fibers. Myofibroblast marker α-SMA stains were significantly elevated in the periductal region. The addition of ursodeoxycholic acid resulted in decreased cholangiocyte injury and reduced fibrosis.
conclusionsBile acid leakage into the submucosa after initial cholangiocyte injury may serve as a possible mechanism of disease propagation and progressive fibrosis in cholangiopathies.
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