ReviewAntioxidants & redox signaling2013
Oxidative stress, redox signaling, and metal chelation in anthracycline cardiotoxicity and pharmacological cardioprotection.
Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.
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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
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 322 citations in OpenAlex.
- A systematic review of the pathophysiology of 5-fluorouracil-induced cardiotoxicity.BMC pharmacology & toxicology · 2014Pooled it
- Pharmacokinetic-pharmacodynamic modelling of acute N-terminal pro B-type natriuretic peptide after doxorubicin infusion in breast cancer.British journal of clinical pharmacology · 2016Trial
- Effect of Remote Ischaemic Conditioning in Oncology Patients Undergoing Chemotherapy: Rationale and Design of the ERIC-ONC Study--A Single-Center, Blinded, Randomized Controlled Trial.Clinical cardiology · 2016Trial
- Bidentate Metal-Binding Motifs in US FDA Approved Small Molecule Drugs.Journal of medicinal chemistry · 2026Review
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- Amifostine Attenuates Doxorubicin-Induced Subacute Hepatic and Renal Toxicity in Rats.International journal of molecular sciences · 2026Article
- Role of ivabradine for anthracycline-induced cardiotoxicity: a meta-analysis.Cardio-oncology (London, England) · 2026Article
- Experimental evaluation of N-acetylcysteine against doxorubicin cardiotoxicity in rats.BMC pharmacology & toxicology · 2026Article
- Biomimetic hybrid membrane-coated nanoparticles loaded with rhein-iron complex enhance ferroptosis and immunotherapy for triple-negative breast cancer.Materials today. Bio · 2026Article
- The multifaceted mechanisms of Tanshinone IIA in doxorubicin-induced cardiotoxicity.Frontiers in medicine · 2026Review
- Quantitative assessment of changes in left ventricular myocardial work and energy loss in HER2-positive breast cancer patients undergoing combination therapy with chemotherapy and targeted treatment using pressure-strain loop and vector flow mapping.Quantitative imaging in medicine and surgery · 2025Article
- Alteration of cardiac energetics and mitochondrial function in doxorubicin‑induced cardiotoxicity: Molecular mechanism and prospective implications (Review).International journal of molecular medicine · 2025Review
- Daunorubicin and its hydroxy metabolite in cardiomyocytes: insights into cellular kinetics, toxicity, DNA damage, and dexrazoxane-induced cardioprotection.Archives of toxicology · 2025Article
- Therapeutic Potential of Ginsenosides in Anthracycline-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2025Review
- Synergistic miRNA Combinations Mitigate Doxorubicin-Induced Cardiotoxicity: Are We Ready for Clinical Translation?JACC. CardioOncology · 2025Article
- Topobexin targets the Topoisomerase II ATPase domain for beta isoform-selective inhibition and anthracycline cardioprotection.Nature communications · 2025Article
- Article
- Doxorubicin-Induced Cardiotoxicity and the Emerging Role of SGLT2 Inhibitors: From Glycemic Control to Cardio-Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Therapeutic potential of synthetic and natural iron chelators against ferroptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Methodological Aspects of μLC-MS/MS for Wide-Scale Proteomic Analysis of Anthracycline-Induced Cardiomyopathy.ACS omega · 2025Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
significanceAnthracyclines (doxorubicin, daunorubicin, or epirubicin) rank among the most effective anticancer drugs, but their clinical usefulness is hampered by the risk of cardiotoxicity. The most feared are the chronic forms of cardiotoxicity, characterized by irreversible cardiac damage and congestive heart failure. Although the pathogenesis of anthracycline cardiotoxicity seems to be complex, the pivotal role has been traditionally attributed to the iron-mediated formation of reactive oxygen species (ROS). In clinics, the bisdioxopiperazine agent dexrazoxane (ICRF-187) reduces the risk of anthracycline cardiotoxicity without a significant effect on response to chemotherapy. The prevailing concept describes dexrazoxane as a prodrug undergoing bioactivation to an iron-chelating agent ADR-925, which may inhibit anthracycline-induced ROS formation and oxidative damage to cardiomyocytes. RECENT ADVANCES: A considerable body of evidence points to mitochondria as the key targets for anthracycline cardiotoxicity, and therefore it could be also crucial for effective cardioprotection. Numerous antioxidants and several iron chelators have been tested in vitro and in vivo with variable outcomes. None of these compounds have matched or even surpassed the effectiveness of dexrazoxane in chronic anthracycline cardiotoxicity settings, despite being stronger chelators and/or antioxidants. CRITICAL ISSUES: The interpretation of many findings is complicated by the heterogeneity of experimental models and frequent employment of acute high-dose treatments with limited translatability to clinical practice. FUTURE DIRECTIONS: Dexrazoxane may be the key to the enigma of anthracycline cardiotoxicity, and therefore it warrants further investigation, including the search for alternative/complementary modes of cardioprotective action beyond simple iron chelation.
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Registered trials
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 OpenQuestion graph.