ArticleFrontiers in pharmacology2025
Thymidine exerts anti-doxorubicin-induced cardiomyopathy effect through the regulation of the PPAR signaling pathways and ferroptosis pathways.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Morroniside Attenuates Doxorubicin-Induced Cardiotoxicity by Activating the PI3K/AKT/Nrf2/HO-1 Pathway to Inhibit Ferroptosis and Oxidative Stress.Journal of biochemical and molecular toxicology · 2026Article
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7 authors.
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Abstract
Introduction: To evaluate the anti-cardiomyopathic activity of thymine (Thy) and to elucidate its mechanism of action. Methods: Transgenic zebrafish with enhanced green fluorescent protein (EGFP)-labelled hearts ( Results: The results indicated that Thy effectively relieved DOX-induced pericardial edema; reversed the effects of DOX on heart rate, stroke volume, SAS rate, ejection fraction, and blood flow velocity; and relieved DOX-induced myocardial ischemia, myocardial cell apoptosis and pathological structural changes in heart tissues. The RT‒qPCR results revealed that Thy regulated the mRNA expression levels of genes related to the PPAR signaling pathway and ferroptosis pathway (such as Discussion: Thy may exert its anti-DOX-induced cardiomyopathy effect through the regulation of the PPAR signaling and ferroptosis pathways.
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