ArticleFrontiers in pharmacology2025
Ophiopogonin D mitigates doxorubicin-induced cardiomyocyte ferroptosis through the β-catenin/GPX4 pathway.
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 4 papers.
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Who cites it
4 citing papers in PubMed.
- Ferroptosis in Doxorubicin-Induced Cardiotoxicity: From Molecular Mechanisms to Therapeutic Strategies and Clinical Management Paradigms.Reviews in cardiovascular medicine · 2026Review
- [Ophiopogonin D alleviates doxorubicin-induced myocardial hypertrophy in mice by activating the β-catenin/FUNDC1/mitophagy axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review.Drug design, development and therapy · 2026Review
- Homocysteine induces ferroptosis in cardiomyocytes by disrupting β-catenin/GPX4 pathway.PloS one · 2025Article
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Authors and funding
4 authors.
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Abstract
Background: The chemotherapeutic agent doxorubicin has the side effect of inducing injury to cardiomyocytes. Ferroptosis plays an essential role in the onset and progression of cardiac injury. Ophiopogonin D is considered the active component of the Chinese herbal medicine Mai Dong, which is commonly used for the treatment of cardiovascular diseases. This study investigates the impact of ophiopogonin D on doxorubicin-induced cardiomyocyte ferroptosis by focusing on the β-catenin/GPX4 signaling pathway. Methods: Mice were injected intraperitoneally with doxorubicin (10 mg/kg) to create a model of cardiotoxicity. Cardiomyocytes exposed to doxorubicin (1 μM) were treated with ophiopogonin D (5 μM). Western blotting was used to detect β-catenin, FTH1, and GPX4. Malondialdehyde (MDA), glutathione (GSH), and Fe Results: Doxorubicin inhibited β-catenin activity and GPX4 expression, promoting cardiomyocyte ferroptosis Conclusion: Ophiopogonin D inhibits cardiomyocyte ferroptosis induced by doxorubicin by restoring the β-catenin/GPX4 signaling pathway.
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