ArticleThe Journal of pathology2025
Platelet C3G protects from liver fibrosis, while enhancing tumor growth through regulation of the immune response.
Article in The Journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Systemic metabolic dysfunction drives platelet-mediated inflammation, fibrogenesis, and hepatocarcinogenesis in metabolic dysfunction-associated steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Rapgef1 paralog-mediated regulation of Wnt/β-catenin signaling orchestrates early embryo tissue patterning and morphogenesis.Cell communication and signaling : CCS · 2026Article
- Deletion of C3G in hepatocytes impairs full liver maturation and alters glucose homeostasis.Cell death & disease · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Primary liver cancer usually occurs in the context of chronic liver disease (CLD), in association with fibrosis. Platelets have emerged as important regulators of CLD and liver cancer, although their precise function and mechanism of action need to be clarified. C3G (RapGEF1) regulates platelet activation, adhesion, and secretion. Here we evaluate the role of platelet C3G in chemically induced fibrosis and liver cancer associated with fibrosis using genetically modified mouse models. We found that while overexpression of full-length C3G in platelets decreased liver fibrosis induced by chronic treatment with CCl
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