ReviewRedox biology2020
Teaching the basics of the mechanism of doxorubicin-induced cardiotoxicity: Have we been barking up the wrong tree?
Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
149 citing papers in PubMed, 4 syntheses or guidelines pooled it, 316 citations in OpenAlex.
- A meta-analysis of risk factors for cardiovascular adverse events with anthracycline based chemotherapy in lymphoma patients.BMC cancer · 2025Pooled it
- Chemotherapy cardiotoxicity research in cancer patients: a bibliometric and visual analysis (1994-2024).Frontiers in oncology · 2025Pooled it
- Natural Killer Cell-Derived Extracellular Vesicles as a Promising Immunotherapeutic Strategy for Cancer: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Efficacy of Physical Exercise to Offset Anthracycline-Induced Cardiotoxicity: A Systematic Review and Meta-Analysis of Clinical and Preclinical Studies.Journal of the American Heart Association · 2021Pooled it
- HydroMg attenuates doxorubicin-induced myocardial injury via promoting mitochondrial function.Medical gas research · 2027Article
- Ankyrin Repeat Domain 1: A Key Regulatory Factor and Emerging Therapeutic Target in Heart Disease.Reviews in cardiovascular medicine · 2026Review
- Doxorubicin-Induced Cardiotoxicity in Breast Cancer: Mechanistic Pathways, Pharmacogenomic Modifiers, and Translational Strategies.Cardiovascular toxicology · 2026Review
- In vivo dynamic nuclear polarization magnetic resonance imaging reveals cardiac mitochondrial redox imbalance as an early indicator of heart failure.Redox biology · 2026Article
- Review
- Chiral metal nanozyme-enabled SOD2 activation and siRNA delivery cooperatively mitigating chronic heart failure.Bioactive materials · 2026Article
- EDTA-Functionalized Nanoscale Metal-Organic Framework for Onco-Cardiology via Radiochemotherapy Synergy and Spatiotemporally Matched Iron Chelation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Enhanced predictive value of post-treatment lymphocyte-based immunoinflammatory biomarkers for cancer therapy-related cardiac dysfunction in anthracycline-treated breast cancer patients.Cardio-oncology (London, England) · 2026Article
- Protective effect of Baicalin against doxorubicin-induced cytotoxic and electrophysiological damage in human iPSC-cardiomyocytes.Scientific reports · 2026Article
- Downregulated TRIM35 Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Inflammation via Inhibiting TLR4/NF-κB Pathway.Cardiovascular drugs and therapy · 2026Article
- Therapeutic potential of Sheng-Xian-Tang in doxorubicin-induced chronic heart failure by regulation of phenylalanine metabolism disruption.Chinese medicine · 2026Article
- Targeting SIRT1 stability: arctiin ameliorates doxorubicin-induced cardiac injury by inhibiting SMURF2 binding and enhancing protective lipid metabolism.Frontiers in pharmacology · 2026Article
- GBVAM as a Novel NHE1 Inhibitor Alleviates Doxorubicin-Induced Cardiotoxicity via PI3K/Akt/mTOR Pathway.Drug design, development and therapy · 2026Article
- FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025Article
- Targeting the NLRP3 by Natural Compounds: Therapeutic Strategies to Mitigate Doxorubicin-Induced Cardiotoxicity.Cell biochemistry and biophysics · 2025Review
- A novel cardioprotective mechanism of rosuvastatin: restoring PINK1/parkin-mediated mitophagy via SIRT1/FOXO1 activation in doxorubicin-induced cardiotoxicity.Cancer chemotherapy and pharmacology · 2025Article
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (DOX), or Adriamycin, an anthracycline antibiotic discovered serendipitously as a chemotherapeutic drug several decades ago, is still one of the most effective drugs for treating various adult and pediatric cancers (breast cancer, Hodgkin's disease, lymphoblastic leukemia). However, one of the major side effects of the continuous use of DOX is dose-dependent, long-term, and potentially lethal cardiovascular toxicity (congestive heart failure and cardiomyopathy) in cancer survivors many years after cessation of chemotherapy. In addition, predisposition to cardiotoxicity varied considerably among individuals. The long-held notion that DOX cardiotoxicity is caused by reactive oxygen species formed from the redox-cycling of DOX semiquinone lacks rigorous proof in a chronic animal model, and administration of reactive oxygen species detoxifying agents failed to reverse DOX-induced cardiac problems. In this review, I discuss the pros and cons of the reactive oxygen species pathway as a primary or secondary mechanism of DOX cardiotoxicity, the role of topoisomerases, and the potential use of mitochondrial-biogenesis-enhancing compounds in reversing DOX-induced cardiomyopathy. New approaches for well-designed clinical trials that repurpose FDA-approved drugs and naturally occurring polyphenolic compounds prophylactically to prevent or mitigate cardiovascular complications in both pediatric and adult cancer survivors are needed. Essentially, the focus should be on enhancing mitochondrial biogenesis to prevent or mitigate DOX-induced cardiotoxicity.
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Identifiers
What OpenQuestion holds
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.