ArticleFrontiers in immunology2025
Bioinformatics based exploration of the anti-liver fibrosis mechanism of Pien Tze Huang via EGFR/JAK1/STAT3 pathway.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Loganin Ameliorates Cholestatic Liver Fibrosis by Inhibiting Hepatic Stellate Cell Autophagy and Activation Through EGFR Signaling.Mediators of inflammation · 2026Article
- Exploring the mechanisms underlying quercetin, a key component ofFrontiers in immunology · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
Object: Liver fibrosis is a key stage in chronic liver disease, but targeted treatments are scarce. Pien Tze Huang (PZH), a traditional Chinese medicine, shows anti-fibrotic potential, though its mechanisms are not fully understood. Method: A liver fibrosis model was created in C57BL/6 mice using carbon tetrachloride (CCL Results: PZH significantly attenuated hepatic transaminase disorders, reduced serum procollagen III/IV, alleviated fibrotic liver histopathology, and suppressed macrophage markers and hepatic inflammation. Through multi-database integration, 24 bioactive compounds were identified in PZH, including ginsenoside Rh2. Further investigation showed that PZH ameliorates liver fibrosis by modulating key targets, including AKT1, EGFR, and STAT3. Molecular docking analysis and molecular dynamics simulation demonstrated a significantly high binding affinity between ginsenoside Rh2 and the target proteins EGFR, JAK1, and STAT3. Conclusion: The findings reveal that PZH ameliorates liver fibrosis by inhibiting macrophage-mediated inflammation via blockade of the EGFR/JAK1/STAT3 signaling axis, providing a mechanistic foundation for its clinical application.
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