ArticleNature communications2021
A human multi-lineage hepatic organoid model for liver fibrosis.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.
- Evolution and hotspots in breast cancer organoid research: insights from a bibliometric and visual knowledge mapping study (2005-2024).Frontiers in oncology · 2025Pooled it
- Liver organoids: From fabrication to application in liver diseases.Frontiers in physiology · 2022Pooled it
- Real-time sensing-integrated organoid-on-a-chip platforms: Technological progress and emerging biomedical applications.Bioactive materials · 2026Review
- A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026Review
- Liver Organoids: From Disease Modelling to Regenerative Medicine.Cell proliferation · 2026Review
- 3D Liver Fibrosis Models in Lab: A Novel Modality for Drug Screening.Pharmacology research & perspectives · 2026Review
- Planar neural organoids as an advanced in vitro model to study patient-derived melanoma metastasis.Scientific reports · 2026Article
- Liver organoids for chemical risk assessment: biological fidelity, standardization, and context-of-use frameworks.Archives of pharmacal research · 2026Review
- Accelerating scientific discovery with Co-Scientist.Nature · 2026Article
- Article
- MagmaFlow: A desktop platform for artificial intelligence-driven expression analysis.FEBS open bio · 2026Article
- P-STAT3-dependent SPP1 transcription in cholangiocytes drives hepatic stellate cells activation in congenital hepatic fibrosis.Communications biology · 2026Article
- Organoids in Pediatric Congenital Hepatobiliary Diseases: Current Status and Progress in Clinical Translational Research.Biomedicines · 2026Review
- Article
- [Advances in the construction and application of a novel liver organoid model for hepatitis B virus infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Modeling hepatic fibrosis in TP53 knockout iPSC-derived human liver organoids.Molecular oncology · 2026Article
- Applications and limitations of pluripotent stem cell-derived liver organoids.Chinese medical journal · 2026Review
- Organoids in Cancer Research and Regenerative Medicine: Current Status, Challenges, and Future Prospects.MedComm · 2026Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
To investigate the pathogenesis of a congenital form of hepatic fibrosis, human hepatic organoids were engineered to express the most common causative mutation for Autosomal Recessive Polycystic Kidney Disease (ARPKD). Here we show that these hepatic organoids develop the key features of ARPKD liver pathology (abnormal bile ducts and fibrosis) in only 21 days. The ARPKD mutation increases collagen abundance and thick collagen fiber production in hepatic organoids, which mirrors ARPKD liver tissue pathology. Transcriptomic and other analyses indicate that the ARPKD mutation generates cholangiocytes with increased TGFβ pathway activation, which are actively involved stimulating myofibroblasts to form collagen fibers. There is also an expansion of collagen-producing myofibroblasts with markedly increased PDGFRB protein expression and an activated STAT3 signaling pathway. Moreover, the transcriptome of ARPKD organoid myofibroblasts resemble those present in commonly occurring forms of liver fibrosis. PDGFRB pathway involvement was confirmed by the anti-fibrotic effect observed when ARPKD organoids were treated with PDGFRB inhibitors. Besides providing insight into the pathogenesis of congenital (and possibly acquired) forms of liver fibrosis, ARPKD organoids could also be used to test the anti-fibrotic efficacy of potential anti-fibrotic therapies.
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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.