ReviewFrontiers in pharmacology2026
Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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
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Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Fibrosis and cancer share epithelial-mesenchymal transition (EMT) as a core pathological driver, making EMT-targeted therapy a promising dual strategy. The natural flavonoid luteolin shows preliminary anti-fibrotic and anti-tumour activities, but its translational potential remains poorly systematized. Methods: We conducted a ConPhyMP compliant systematic review, searching PubMed for 2008-2026 studies on luteolin and its derivatives, EMT, fibrosis and cancer, to synthesize evidence on their mechanisms, efficacy and translational prospects. Results: Luteolin inhibits EMT via multi-target regulation of core pathways (TGF-β1/Smad, PI3K/Akt, Hippo/YAP), exerting consistent dose-dependent efficacy in suppressing cancer metastasis and multi-organ fibrosis. Structural modifications and nanodelivery systems resolved its bioavailability limitations, and rigorous validation ruled out pan-assay interference compounds (PAINS). Conclusion: Luteolin and its derivatives are promising dual-effect EMT-targeted therapeutics. Optimized formulations lay the groundwork for clinical translation, and future large-scale trials are needed to validate their clinical efficacy.
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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 Socratic graph.