ArticleMolecular biology reports2024
Inhibition of cytochrome P450 epoxygenase promotes endothelium-to-mesenchymal transition and exacerbates doxorubicin-induced cardiovascular toxicity.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Anthracyclines-Induced Vascular Endothelial Dysfunction in Cancer Patients and Survivors Using Brachial Flow-Mediated Dilation (FMD) Tool: A Systematic Review and Meta-Analysis.Cardiovascular toxicology · 2025Pooled it
- PTUPB, a soluble epoxide hydrolase/cyclooxygenase‑2 dual inhibitor, reduces endothelial‑to‑mesenchymal transition and improves doxorubicin‑induced vascular and cardiac toxicity.Molecular medicine reports · 2026Article
- Integrated Omics Approach to Delineate the Mechanisms of Doxorubicin-Induced Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Role of Perindopril in Mitigating Doxorubicin's Vascular Toxicity in a Rat Model.Cardiovascular toxicology · 2026Article
- Comparative proteomic analysis of colorectal cancer stem cells reveals potential biomarkers and altered pathways.Frontiers in molecular biosciences · 2026Article
- Expression profiling of inhibitory immune checkpoints in colorectal cancer stem cells and their association with tumor immunity and immunotherapy biomarkers.Frontiers in immunology · 2026Article
- Integrative network toxicology, molecular dynamics and transcriptional analysis elucidate DEHP-induced cardiovascular dysfunction.Toxicology research · 2025Article
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Astragalus Injection Modulates the Pharmacokinetics of Doxorubicin and CYP450 Enzymes.Current pharmaceutical design · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundDoxorubicin (DOX) is a potent chemotherapy widely used in treating various neoplastic diseases. However, the clinical use of DOX is limited due to its potential toxic effect on the cardiovascular system. Thus, identifying the pathway involved in this toxicity may help minimize chemotherapy risk and improve cancer patients' quality of life. Recent studies suggest that Endothelial-to-Mesenchymal transition (EndMT) and endothelial toxicity contribute to the pathogenesis of DOX-induced cardiovascular toxicity. However, the molecular mechanism is yet unknown. Given that arachidonic acid and associated cytochrome P450 (CYP) epoxygenase have been involved in endothelial and cardiovascular function, we aimed to examine the effect of suppressing CYP epoxygenases on DOX-induced EndMT and cardiovascular toxicity in vitro and in vivo. METHODS AND
resultsTo test this, human endothelial cells were treated with DOX, with or without CYP epoxygenase inhibitor, MSPPOH. We also investigated the effect of MSPPOH on the cardiovascular system in our zebrafish model of DOX-induced cardiotoxicity. Our results showed that MSPPOH exacerbated DOX-induced EndMT, inflammation, oxidative stress, and apoptosis in our endothelial cells. Furthermore, we also show that MSPPOH increased cardiac edema, lowered vascular blood flow velocity, and worsened the expression of EndMT and cardiac injury markers in our zebrafish model of DOX-induced cardiotoxicity.
conclusionOur data indicate that a selective CYP epoxygenase inhibitor, MSPPOH, induces EndMT and endothelial toxicity to contribute to DOX-induced cardiovascular toxicity.
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