ArticleProceedings of the National Academy of Sciences of the United States of America2014
Origin of myofibroblasts in the fibrotic liver in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers, 1 of them a synthesis 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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
305 citing papers in PubMed, 1 synthesis or guideline pooled it, 527 citations in OpenAlex.
- Research reviews and prospects of gut microbiota in liver cirrhosis: a bibliometric analysis (2001-2023).Frontiers in microbiology · 2024Pooled it
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- Hepatocyte CD146 and soluble CD146 promote hepatic stellate cell activation via the integrin αvβ1-p38 MAPK signaling axis to drive liver fibrosis.Cellular and molecular life sciences : CMLS · 2026Article
- Shared mechanisms of organ fibrosis.JCI insight · 2026Review
- Pulmonary fibroblast subsets demonstrate differentially enriched signaling pathways during fibrosis resolution and repair.JCI insight · 2026Article
- Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.JCI insight · 2026Review
- Rutin attenuates liver fibrosis via the IRG1-itaconate-Nrf2 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- USP13 promotes hepatic stellate cells activation and aggravates liver fibrosis through deubiquitinating SMAD3.Hepatology international · 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
- COX2Physiological reports · 2026Article
- Clec3b⁺ fibroblasts are the primary effectors of portal fibrosis following activation via a KLF4/periostin axis.Nature communications · 2026Article
- Zearalenone Promotes Hepatic Stellate Cell Activation and Early Profibrotic Tendency in the Liver.Biomolecules · 2026Article
- Nanozymes for Liver Disease Therapy: Advances in Catalytic Activity, Targeting Strategies, and Clinical Translation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- A robust mouse liver organoid platform enables sustained multicellular maturation and fibrosis modeling from a single tissue sample.Scientific reports · 2026Article
- ECM1 produced by hepatic stellate cells serves as a gatekeeper of liver homeostasis in hepatic fibrosis.Hepatology (Baltimore, Md.) · 2026Article
- HMGB1-mediated enhancement of glycolysis activates hepatic stellate cells by inhibiting ferroptosis in alcoholic hepatic fibrosis.Stem cell research & therapy · 2026Article
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026Review
- Hepatic Stellate Cell-derived IL-11 Exacerbates Liver Fibrosis via Interplay between HSCs and Macrophages.International journal of biological sciences · 2026Article
245 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
18 authors at 7 institutions in 4 countries.
Funding
Abstract
Hepatic myofibroblasts are activated in response to chronic liver injury of any etiology to produce a fibrous scar. Despite extensive studies, the origin of myofibroblasts in different types of fibrotic liver diseases is unresolved. To identify distinct populations of myofibroblasts and quantify their contribution to hepatic fibrosis of two different etiologies, collagen-α1(I)-GFP mice were subjected to hepatotoxic (carbon tetrachloride; CCl4) or cholestatic (bile duct ligation; BDL) liver injury. All myofibroblasts were purified by flow cytometry of GFP(+) cells and then different subsets identified by phenotyping. Liver resident activated hepatic stellate cells (aHSCs) and activated portal fibroblasts (aPFs) are the major source (>95%) of fibrogenic myofibroblasts in these models of liver fibrosis in mice. As previously reported using other methodologies, hepatic stellate cells (HSCs) are the major source of myofibroblasts (>87%) in CCl4 liver injury. However, aPFs are a major source of myofibroblasts in cholestatic liver injury, contributing >70% of myofibroblasts at the onset of injury (5 d BDL). The relative contribution of aPFs decreases with progressive injury, as HSCs become activated and contribute to the myofibroblast population (14 and 20 d BDL). Unlike aHSCs, aPFs respond to stimulation with taurocholic acid and IL-25 by induction of collagen-α1(I) and IL-13, respectively. Furthermore, BDL-activated PFs express high levels of collagen type I and provide stimulatory signals to HSCs. Gene expression analysis identified several novel markers of aPFs, including a mesothelial-specific marker mesothelin. PFs may play a critical role in the pathogenesis of cholestatic liver fibrosis and, therefore, serve as an attractive 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.