ArticleProceedings of the National Academy of Sciences of the United States of America2013
Mesothelial cells give rise to hepatic stellate cells and myofibroblasts via mesothelial-mesenchymal transition in liver injury.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
What it found
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Who cites it
131 citing papers in PubMed, 208 citations in OpenAlex.
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- Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.JCI insight · 2026Review
- Organ-Specific and Conserved Regulatory Logic Orchestrates Gene Expression in the Embryonic Mesothelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- COX2Physiological reports · 2026Article
- Global Trends in Hepatocellular Carcinoma and TGF-β Research: A Bibliometric and Visualization Analysis from 2000 to 2024.Current protein & peptide science · 2026Article
- Hepatic stellate cells in liver fibrosis: From biology to pathology.Open veterinary journal · 2025Review
- Interleukin-18 binding protein protects against metabolic steatohepatitis.Hepatology communications · 2025Article
- A comprehensive molecular atlas of the mesenchymal cell types in the mouse liver.EMBO reports · 2025Article
- Combined pharmacological targeting of CD9Cell reports. Medicine · 2025Article
- Hepatic stellate cells: balancing homeostasis, hepatoprotection and fibrogenesis in health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Dynamic WT1 expression during gastrulation specifies peritoneal smooth muscle fate independently of mesothelial fate.Development (Cambridge, England) · 2025Article
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- Tissue adhesion after surgical interventions (Review).Experimental and therapeutic medicine · 2025Review
- Periductal fibroblasts participate in liver homeostasis, fibrosis, and tumorigenesis.The Journal of experimental medicine · 2025Article
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Cancer-associated fibroblasts in hepatocellular carcinoma: origins, heterogeneity, and therapeutic implications.Frontiers in immunology · 2025Review
- Article
- Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
71 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
3 authors at 1 institution in 1 country.
Funding
Abstract
In many organs, myofibroblasts play a major role in the scarring process in response to injury. In liver fibrogenesis, hepatic stellate cells (HSCs) are thought to transdifferentiate into myofibroblasts, but the origins of both HSCs and myofibroblasts remain elusive. In the developing liver, lung, and intestine, mesothelial cells (MCs) differentiate into specific mesenchymal cell types; however, the contribution of this differentiation to organ injury is unknown. In the present study, using mouse models, conditional cell lineage analysis has demonstrated that MCs expressing Wilms tumor 1 give rise to HSCs and myofibroblasts during liver fibrogenesis. Primary MCs, isolated from adult mouse liver using antibodies against glycoprotein M6a, undergo myofibroblastic transdifferentiation. Antagonism of TGF-β signaling suppresses transition of MCs to mesenchymal cells both in vitro and in vivo. These results indicate that MCs undergo mesothelial-mesenchymal transition and participate in liver injury via differentiation to HSCs and myofibroblasts.
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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.