ReviewBiochimica et biophysica acta. Molecular basis of disease2018
Mechanisms of cholangiocyte responses to injury.
Review in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 92 citations in OpenAlex.
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Biliary Microbiota in Health and Disease: Clinical Implications in Lithiasis, Infection, and Antimicrobial Resistance.Antibiotics (Basel, Switzerland) · 2026Review
- Adipose-Derived Stem Cell Treatment Induces Early-Term Hes1 Upregulation in a Sox9- and Notch1-Independent Manner in a Rat Model of Bile Duct Ligation.Biomedicines · 2026Article
- Microbiome-derived bile acids as endogenous regenerative mediators in liver repair.Regenerative therapy · 2025Review
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Review
- Review
- Cell-Type Deconvolution Reveals Dynamic Changes in MASLD.Liver international communications · 2025Article
- Cholangiocyte organoids to study drug-induced injury.Stem cell research & therapy · 2024Article
- The pivotal role of dysregulated autophagy in the progression of non-alcoholic fatty liver disease.Frontiers in endocrinology · 2024Review
- Overcoming treatment resistance in cholangiocarcinoma: current strategies, challenges, and prospects.Frontiers in cell and developmental biology · 2024Review
- Clonorchis sinensis granulin promotes malignant transformation of human intrahepatic biliary epithelial cells through interaction with M2 macrophages via regulation of STAT3 phosphorylation and the MEK/ERK pathway.Parasites & vectors · 2023Article
- Bile Acids and Biliary Fibrosis.Cells · 2023Review
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- Pathophysiological Roles of Ductular Reaction in Liver Inflammation and Hepatic Fibrogenesis.Cellular and molecular gastroenterology and hepatology · 2023Article
- Survey ofJournal of animal science and technology · 2022Article
- Role of YAP1 Signaling in Biliary Development, Repair, and Disease.Seminars in liver disease · 2022Review
- Metabolomics- and systems toxicology-based hepatotoxicity mechanism ofFrontiers in pharmacology · 2022Article
- Csi-let-7a-5p delivered by extracellular vesicles from a liver fluke activates M1-like macrophages and exacerbates biliary injuries.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Feedback Signaling between Cholangiopathies, Ductular Reaction, and Non-Alcoholic Fatty Liver Disease.Cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cholangiocytes, epithelial cells that line the biliary epithelium, are the primary target cells for cholangiopathies including primary sclerosing cholangitis and primary biliary cholangitis. Quiescent cholangiocytes respond to biliary damage and acquire an activated neuroendocrine phenotype to maintain the homeostasis of the liver. The typical response of cholangiocytes is proliferation leading to bile duct hyperplasia, which is a characteristic of cholestatic liver diseases. Current studies have identified various signaling pathways that are associated with cholangiocyte proliferation/loss and liver fibrosis in cholangiopathies using human samples and rodent models. Although recent studies have demonstrated that extracellular vesicles and microRNAs could be mediators that regulate these messenger/receptor axes, further studies are required to confirm their roles. This review summarizes current studies of biliary response and cholangiocyte proliferation during cholestatic liver injury with particular emphasis on the secretin/secretin receptor axis. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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.