ArticleCell death & disease2020
Myofibroblast induces hepatocyte-to-ductal metaplasia via laminin-ɑvβ6 integrin in liver fibrosis.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular PET imaging of integrin αvβ6 reveals biliary and fibrotic changes in preclinical MASH.Biomarker research · 2026Article
- Liver portal fibroblasts induce the functions of primary human hepatocytes in vitro.Communications biology · 2025Article
- Nanomedicines in the Treatment of Liver Fibrosis: A Review.International journal of nanomedicine · 2025Review
- Interferon-γ secreted by recruited Th1 cells in peritoneal cavity inhibits the formation of malignant ascites.Cell death discovery · 2023Article
- New insights into fibrotic signaling in hepatocellular carcinoma.Frontiers in oncology · 2023Review
- Role of Immune Cells in Biliary Repair.Frontiers in immunology · 2022Review
- A Dynamic Transcriptome Map of Different Tissue Microenvironment Cells Identified During Gastric Cancer Development Using Single-Cell RNA Sequencing.Frontiers in immunology · 2021Article
- Resident Fibroblast MKL1 Is Sufficient to Drive Pro-fibrogenic Response in Mice.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocytes undergo the metaplasia into ductal biliary epithelial cells (BECs) in response to chronic injury, and subsequently contribute to liver regeneration. The mechanism underlying hepatocyte-to-ductal metaplasia has not been explored until now. In mouse models of liver fibrosis, a florid BEC response was observed in fibrotic liver, and the depletion of myofibroblasts attenuated BEC expansion remarkably. Then, in hepatocyte fate-tracing mouse model, we demonstrated the conversion of mature hepatocytes into ductal BECs in fibrotic liver, and the depletion of myofibroblasts diminished the hepatocyte-to-ductal metaplasia. Finally, the mechanism underlying the metaplasia was investigated. Myofibroblasts secreted laminin-rich extracellular matrix, and then laminin induced hepatocyte-to-ductal metaplasia through ɑvβ6 integrin. Therefore, our results demonstrated myofibroblasts induce the conversion of mature hepatocytes into ductal BECs through laminin-ɑvβ6 integrin, which reveals that the strategy improve regeneration in fibrotic liver through the modification of specific microenvironment.
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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.