ArticleThe Journal of clinical investigation2017
Mesothelin/mucin 16 signaling in activated portal fibroblasts regulates cholestatic liver fibrosis.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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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.
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Who cites it
76 citing papers in PubMed, 103 citations in OpenAlex.
- Review
- MSLN expression predicts a high risk of EMD in AML by promoting cell adhesion and metastasis via interaction with MUC16.Blood advances · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation.Journal of translational medicine · 2026Review
- Zearalenone Promotes Hepatic Stellate Cell Activation and Early Profibrotic Tendency in the Liver.Biomolecules · 2026Article
- A monoclonal antibody W1 blocks mesothelin-mediated tumor progression.Molecular therapy. Oncology · 2026Article
- Mesothelin biology and the evolving landscape of targeted immunotherapy.Molecular therapy. Oncology · 2026Review
- Portal Fibroblasts: A Hidden Driver of Cholestasis-Associated Liver Cancer.Cellular and molecular gastroenterology and hepatology · 2026Article
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Hepatic Stellate Cell-derived IL-11 Exacerbates Liver Fibrosis via Interplay between HSCs and Macrophages.International journal of biological sciences · 2026Article
- Mesothelin/Mucin 16 Signaling in Activated Portal Fibroblasts Drives the Development of Cholestatic Fibrosis and Hepatocellular Carcinoma in Aged Female Multidrug Resistance Protein 2 Knockout Mice.Cellular and molecular gastroenterology and hepatology · 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
- Global Trends in Hepatocellular Carcinoma and TGF-β Research: A Bibliometric and Visualization Analysis from 2000 to 2024.Current protein & peptide science · 2026Article
- Novel perspectives on MSLN-targeted cancer therapy: from molecular mechanisms to clinical translation.Cancer biology & therapy · 2025Review
- EMP1 + hepatic stellate cells drive hepatic fibrosis progression to hepatocellular carcinoma and predict prognosis.Journal of translational medicine · 2025Article
- Mesothelin as a biomarker and potential therapeutic target in rheumatoid arthritis bone destruction.Cell reports. Medicine · 2025Article
- Microbiome dysbiosis, neutrophil recruitment and mesenchymal transition of mesothelial cells promotes peritoneal metastasis of colorectal cancer.Nature cancer · 2025Article
- A Golden Shield: The Protective Role of Curcumin against Liver Fibrosis.Current medicinal chemistry · 2025Review
- Deciphering the Role of Oroxylin A in Liver Fibrosis.Drug design, development and therapy · 2025Review
- Identification and Validation of Key Genes Involved in the Coupling of Mitochondria-Associated Endoplasmic Reticulum Membrane in Hemorrhoidal Disease.International journal of general medicine · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
Cholestatic liver fibrosis is caused by obstruction of the biliary tract and is associated with early activation of portal fibroblasts (PFs) that express Thy-1, fibulin 2, and the recently identified marker mesothelin (MSLN). Here, we have demonstrated that activated PFs (aPFs) and myofibroblasts play a critical role in the pathogenesis of liver fibrosis induced by bile duct ligation (BDL). Conditional ablation of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately 50%. Similar results were observed in MSLN-deficient mice (Msln-/- mice) or mice deficient in the MSLN ligand mucin 16 (Muc16-/- mice). In vitro analysis revealed that MSLN regulates TGF-β1-inducible activation of WT PFs by disrupting the formation of an inhibitory Thy-1-TGFβRI complex. MSLN also facilitated the FGF-mediated proliferation of WT aPFs. Therapeutic administration of anti-MSLN-blocking Abs attenuated BDL-induced fibrosis in WT mice. Liver specimens from patients with cholestatic liver fibrosis had increased numbers of MSLN+ aPFs/myofibroblasts, suggesting that MSLN may be a potential target for antifibrotic therapy.
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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.