ReviewClinical science (London, England : 1979)2021
Molecular mechanisms of anthracycline cardiovascular toxicity.
Review in Clinical science (London, England : 1979), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
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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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- The influence of sodium-glucose co-transporter-2 inhibitors on the risk of cancer therapy-related cardiac dysfunction: A meta-analysis.Biomolecules & biomedicine · 2025Pooled it
- Predictive value of left ventricularAnnals of nuclear medicine · 2026Article
- Endothelial Injury as a Potential Contributor to Cardiovascular Toxicity in Hematologic Malignancies.Diseases (Basel, Switzerland) · 2026Review
- Early cardiac proteomic profiling in a long-latency doxorubicin cardiomyopathy model exhibits sexual dimorphism for cardioprotection.Journal of molecular and cellular cardiology plus · 2026Article
- Chemotherapy-Induced Right Ventricular Dysfunction.Medicina (Kaunas, Lithuania) · 2026Review
- The MASLD-Cardio-Oncology Triangle: Dietary Patterns, Metabolic Remodelling and Implications for Cancer Therapy Tolerance.Nutrients · 2026Review
- Vardenafil Alleviates Doxorubicin-Induced Cardiotoxicity Associated with Restoration of the AMPK/SIRT1 Signaling Pathway.Biomedicines · 2026Article
- Anthraquinone-Loaded Liposomes for TAM Reprogramming in Triple-Negative Breast Cancer: Mechanistic Rationale, Delivery Logic, and Translational Challenges.Pharmaceutics · 2026Review
- Environmental endocrine disruptors in cardio-oncology: emerging modifiers of cardiovascular vulnerability in patients with cancer.Cardio-oncology (London, England) · 2026Review
- Trabectedin-Associated Myocardial Infarction With Nonobstructive Coronary Arteries.JACC. Case reports · 2026Article
- Article
- Role of ivabradine for anthracycline-induced cardiotoxicity: a meta-analysis.Cardio-oncology (London, England) · 2026Article
- Ferroptosis in cardiovascular diseases: molecular mechanisms and a novel therapeutic target.Molecular biomedicine · 2026Review
- Post-marketing safety evaluation of anthracycline for acute myeloid leukemia treatment: a real-world pharmacovigilance analysis.Frontiers in pharmacology · 2026Article
- Cardiotoxicity associated with anticancer therapies for gynecological tumors.Frontiers in cardiovascular medicine · 2026Review
- Cardiac safety of L-Annamycin: a pooled analysis of five clinical trials.Frontiers in cardiovascular medicine · 2026Article
- Engineering Human 3D Cardiac Tissues for Predictive Functional Drug Screening.Pharmaceutics · 2025Article
- Article
- Structure, biological activity, and biosynthesis of natural chromanes and chromenes.Archives of pharmacal research · 2025Review
- A Comprehensive Overview on Chemotherapy-Induced Cardiotoxicity: Insights into the Underlying Inflammatory and Oxidative Mechanisms.Cardiovascular drugs and therapy · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Anthracyclines are effective chemotherapeutic agents, commonly used in the treatment of a variety of hematologic malignancies and solid tumors. However, their use is associated with a significant risk of cardiovascular toxicities and may result in cardiomyopathy and heart failure. Cardiomyocyte toxicity occurs via multiple molecular mechanisms, including topoisomerase II-mediated DNA double-strand breaks and reactive oxygen species (ROS) formation via effects on the mitochondrial electron transport chain, NADPH oxidases (NOXs), and nitric oxide synthases (NOSs). Excess ROS may cause mitochondrial dysfunction, endoplasmic reticulum stress, calcium release, and DNA damage, which may result in cardiomyocyte dysfunction or cell death. These pathophysiologic mechanisms cause tissue-level manifestations, including characteristic histopathologic changes (myocyte vacuolization, myofibrillar loss, and cell death), atrophy and fibrosis, and organ-level manifestations including cardiac contractile dysfunction and vascular dysfunction. In addition, these mechanisms are relevant to current and emerging strategies to diagnose, prevent, and treat anthracycline-induced cardiomyopathy. This review details the established and emerging data regarding the molecular mechanisms of anthracycline-induced cardiovascular toxicity.
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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.