ReviewFrontiers in molecular biosciences2021
The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis.
Review in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Mesothelin biology and the evolving landscape of targeted immunotherapy.Molecular therapy. Oncology · 2026Review
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Decoding the role of mesothelin in tumor dynamics and targeted treatment innovations.Molecular biomedicine · 2025Review
- Single-Nucleus RNA Sequencing and Spatial Transcriptomics Reveal Cellular Heterogeneity and Intercellular Communication Networks in the Hypothalamus-Pituitary-Ovarian Axis of Pregnant Mongolian Cattle.Animals : an open access journal from MDPI · 2025Article
- Liver portal fibroblasts induce the functions of primary human hepatocytes in vitro.Communications biology · 2025Article
- The possible pathogenesis of liver fibrosis: therapeutic potential of natural polyphenols.Pharmacological reports : PR · 2024Review
- Fate tracking reveals differences between ReelinCell proliferation · 2023Article
- Cellular and Molecular Mechanisms of Toxic Liver Fibrosis in Rats Depending on the Stages of Its Development.Sovremennye tekhnologii v meditsine · 2023Article
- The Role of Mesothelin in Activation of Portal Fibroblasts in Cholestatic Liver Injury.Biology · 2022Review
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Liver fibrosis develops in response to chronic toxic or cholestatic injury, and is characterized by apoptosis of damaged hepatocytes, development of inflammatory responses, and activation of Collagen Type I producing myofibroblasts that make liver fibrotic. Two major cell types, Hepatic Stellate Cells (HSCs) and Portal Fibroblasts (PFs) are the major source of hepatic myofibroblasts. Hepatotoxic liver injury activates Hepatic Stellate Cells (aHSCs) to become myofibroblasts, while cholestatic liver injury activates both aHSCs and Portal Fibroblasts (aPFs). aPFs comprise the major population of myofibroblasts at the onset of cholestatic injury, while aHSCs are increasingly activated with fibrosis progression. Here we summarize our current understanding of the role of aPFs in the pathogenesis of cholestatic fibrosis, their unique features, and outline the potential mechanism of targeting aPFs in fibrotic liver.
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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.