ArticleRedox biology2024
Pharmacological activation of GPX4 ameliorates doxorubicin-induced cardiomyopathy.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Incretin-Based Therapies in Doxorubicin-Induced Cardiotoxicity: A Systematic Review of GLP-1 and Dual GIP/GLP-1 Agonists.Cardiovascular toxicology · 2026Pooled it
- Supramolecular Chiral Assemblies from Benzoselenadiazole-Alanine-Acylhydrazone Conjugates Enable Cardioprotection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- Neuroprotective Potential of Peptide KSVSPKFLTG fromAntioxidants (Basel, Switzerland) · 2026Article
- GIPC1 governed ferroptosis by regulating DECR1-modulating lipid homeostasis during dilated cardiomyopathy (DCM).Cell death and differentiation · 2026Article
- Ferroptosis in Doxorubicin-Induced Cardiotoxicity: From Molecular Mechanisms to Therapeutic Strategies and Clinical Management Paradigms.Reviews in cardiovascular medicine · 2026Review
- CD74 deficiency protects against doxorubicin cardiotoxicity through RRM2-mediated regulation of ferroptosis.Acta pharmaceutica Sinica. B · 2026Article
- Cysteine imaging reveals early redox dysregulation and identifies gnetol as a ferroptosis-modulating agent in doxorubicin cardiotoxicity.Redox biology · 2026Article
- A facile polysaccharide hydrogel activates PPARγ via the Gut-Kidney axis to ameliorate chronic kidney disease.Journal of nanobiotechnology · 2026Article
- Hyperoside Inhibits Doxorubicin-Induced Ferroptosis in Cardiomyocytes via the Nrf2/GPX4 Pathway.Journal of cardiovascular translational research · 2026Article
- Core Neuroinflammatory Pathways Contributing to Delayed Encephalopathy After Acute Carbon Monoxide Poisoning Revealed by Multi-omics and Single Nucleus RNA-Seq.Current medicinal chemistry · 2026Article
- Ferroptosis inhibitors: mechanisms of action and therapeutic potential.Cellular and molecular life sciences : CMLS · 2025Review
- Faecalibacterium prausnitzii prevents age-related heart failure by suppressing ferroptosis in cardiomyocytes through butyrate-mediated LCN2 regulation.Gut microbes · 2025Article
- Review
- Co-targeting ferroptosis and immune evasion through small molecules in breast cancer.Journal of translational internal medicine · 2025Article
- NEDD4L-Mediated Ubiquitination of GPX4 Exacerbates Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Article
- Article
- H 2 protects H9c2 cells from hypoxia/reoxygenation injury by inhibiting the Wnt/CX3CR1 signaling pathway.Medical gas research · 2025Article
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- Multifaced Anticancer Potential of Doxorubicin: Spotlight on Breast Cancer.Diseases & research · 2025Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to the cardiotoxicity of doxorubicin (DOX), its clinical application is limited. Lipid peroxidation caused by excessive ferrous iron is believed to be a key molecular mechanism of DOX-induced cardiomyopathy (DIC). Dexrazoxane (DXZ), an iron chelator, is the only drug approved by the FDA for reducing DIC, but it has many side effects and cannot be used as a preventive drug in clinical practice. Single-nucleus RNA sequencing (snRNA-seq) analysis identified myocardial and epithelial cells that are susceptible to DOX-induced ferroptosis. The glutathione peroxidase 4 (GPX4) activator selenomethione (SeMet) significantly reduced polyunsaturated fatty acids (PUFAs) and oxidized lipid levels in vitro. Consistently, SeMet significantly decreased DOX-induced lipid peroxidation in H9C2 cells and mortality in C57BL/6 mice compared to DXZ, ferrostatin-1, and normal saline. SeMet can effectively reduce serum markers of cardiac injury in C57BL/6 mice and breast cancer patients. Depletion of the GPX4 gene in C57BL/6 mice resulted in an increase in polyunsaturated fatty acid (PUFA) levels and eliminated the protective effect of SeMet against DIC. Notably, SeMet exerted antitumor effects on breast cancer models with DOX while providing cardiac protection for the same animal without detectable toxicities. These findings suggest that pharmacological activation of GPX4 is a valuable and promising strategy for preventing the cardiotoxicity of doxorubicin.
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