ReviewStem cells international2016
Revisiting Epithelial-to-Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the "Reactive" Biliary Epithelial Phenotype.
Review in Stem cells international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 54 citations in OpenAlex.
- Melatonin Alleviates Graft Biliary Fibrosis by Inhibiting VIMAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Inhibition of Wnt signaling in primary human hepatocytes promotes Plasmodium falciparum liver stage development.PLoS pathogens · 2025Article
- Mechanisms and targeted prevention of abnormal ductular reaction caused by a low concentration of Benzo(a)pyrene.Cell death & disease · 2025Article
- Anti-fibrotic effect of human amniotic fluid stem cells in biliary epithelial-mesenchymal transition of liver ductal organoid.Stem cells translational medicine · 2025Article
- The transcriptional regulators GATA6 and TET1 regulate the TGF-β pathway in cancer-associated fibroblasts to promote breast cancer progression.Cell death discovery · 2025Article
- Purinergic signaling and cholangiocyte regeneration: a new frontier in ischemic liver injury.Frontiers in transplantation · 2025Review
- Establishment and long-term expansion of adult hepatobiliary organoids co-cultured with liver endothelial cells.Heliyon · 2024Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- BM-MSCs overexpressing the Numb enhance the therapeutic effect on cholestatic liver fibrosis by inhibiting the ductular reaction.Stem cell research & therapy · 2023Article
- Current view of liver cancer cell-of-origin and proposed mechanisms precluding its proper determination.Cancer cell international · 2023Review
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- Characteristics of SOX9-positive progenitor-like cells during cholestatic liver regeneration in biliary atresia.Stem cell research & therapy · 2022Article
- Dual inhibition of TGFβR and ROCK reverses the epithelial to mesenchymal transition in collectively migrating zebrafish keratocytes.Cell biology international · 2021Article
- Article
- The Potentiality of Herbal Remedies in Primary Sclerosing Cholangitis: FromFrontiers in pharmacology · 2020Review
- Knockdown of vimentin reduces mesenchymal phenotype of cholangiocytes in the Mdr2EBioMedicine · 2019Article
- A critical role of autophagy in regulating the mesenchymal transition of ductular cells in liver cirrhosis.Scientific reports · 2019Article
- miR-219-3p regulates the occurrence of hepatic fibrosis by targeting Smad2.Experimental and therapeutic medicine · 2019Article
- Cholangiocyte pathobiology.Nature reviews. Gastroenterology & hepatology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whether liver epithelial cells contribute to the development of hepatic scarring by undergoing epithelial-to-mesenchymal transition (EMT) is a controversial issue. Herein, we revisit the concept of EMT in cholangiopathies, a group of severe hepatic disorders primarily targeting the bile duct epithelial cell (cholangiocyte), leading to progressive portal fibrosis, the main determinant of liver disease progression. Unfortunately, therapies able to halt this process are currently lacking. In cholangiopathies, fibrogenesis is part of ductular reaction, a reparative complex involving epithelial, mesenchymal, and inflammatory cells. Ductular reactive cells (DRC) are cholangiocytes derived from the activation of the hepatic progenitor cell compartment. These cells are arranged into irregular strings and express a "reactive" phenotype, which enables them to extensively crosstalk with the other components of ductular reaction. We will first discuss EMT in liver morphogenesis and then highlight how some of these developmental programs are partly reactivated in DRC. Evidence for "bona fide" EMT changes in cholangiocytes is lacking, but expression of some mesenchymal markers represents a fundamental repair mechanism in response to chronic biliary damage with potential harmful fibrogenetic effects. Understanding microenvironmental cues and signaling perturbations promoting these changes in DRC may help to identify potential targets for new antifibrotic therapies in cholangiopathies.
Identifiers
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.