ArticleNature communications2025
Cellular crosstalk mediated by TGF-β drives epithelial-mesenchymal transition in patient-derived multi-compartment biliary organoids.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A Spatiotemporal Single-Cell Atlas Uncovers Dysregulated ECM Dynamics and Septal Remodeling Arrest in Human Ventricular Septal Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Melatonin Alleviates Graft Biliary Fibrosis by Inhibiting VIMAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The application progress of organoid technology in the toxicity assessment of environmental pollutants.Cell biology and toxicology · 2026Review
- Organoids in Pediatric Congenital Hepatobiliary Diseases: Current Status and Progress in Clinical Translational Research.Biomedicines · 2026Review
- Targeting FGG alleviates cholestatic fibrosis by inhibiting hepatic stellate cell activation and regulating macrophage homeostasis.Journal of nanobiotechnology · 2026Article
- Conserved Ductular Reaction Mechanisms in Biliary Atresia and Primary Sclerosing Cholangitis Derived From Single-Cell and Spatial Transcriptomics.Cellular and molecular gastroenterology and hepatology · 2026Review
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Elevated Epithelial Splicing Regulatory Protein 1 Expression in Biliary Atresia Indicates Its Potential as a Molecular Marker.Biomolecules · 2025Article
- Liver-bone organoids reveal senescence-driven interorgan crosstalk.Bioactive materials · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Deficiencies in the development of epithelial structures and delays in cellular maturation can increase the susceptibility of neonates to disease early in life. To investigate human biliary development and its vulnerability to biliary atresia, a severe pediatric cholangiopathy, we engineered multi-compartment biliary organoids (MBOs) from co-cultures of human liver-derived epithelial organoid cells with human endothelial and mesenchymal cells. MBOs derived from normal livers effectively replicated the epithelial structure of the bile duct epithelium and peribiliary glands (PBGs). Conversely, MBOs from diseased livers exhibited defective epithelial layers, a significant epithelial-mesenchymal transition (EMT), and an activation of the TGF-β/Activin-SMAD2/3 signaling, primarily due to intermediary cell sub-populations. Inhibition of TGF-β signaling suppressed EMT and promoted biliary epithelial development in human MBOs and suppressed the phenotype of experimental biliary atresia in neonatal mice. Thus, the modulation of TGF-β-dependent EMT regulates bile duct epithelial development and influences the susceptibility of neonates to biliary injuries.
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