ReviewClinical and translational science2021
Epigenetic Changes Associated With Anthracycline-Induced Cardiotoxicity.
Review in Clinical and translational science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 27 citations in OpenAlex.
- Role of ivabradine for anthracycline-induced cardiotoxicity: a meta-analysis.Cardio-oncology (London, England) · 2026Article
- Methylated PIH1D1 as a Heart-Specific Biomarker for Anthracycline-Induced Cardiac Remodeling in Breast Cancer Patients.JACC. Basic to translational science · 2026Article
- Cardioprotective strategies of ACEi/ARBs and beta-blockers against anthracycline-induced cardiotoxicity in pediatric cancer survivors: a systematic review.Cardio-oncology (London, England) · 2026Review
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Biochanin A attenuates doxorubicin-induced cardiotoxicity in rats with associated modulation of PI3K/Akt/mTOR and p38 MAPK signaling.Frontiers in cardiovascular medicine · 2026Article
- CPX-351 vs. conventional chemotherapy cardiotoxicity in high-risk AML: a post hoc phase III trial analysis.Cardio-oncology (London, England) · 2025Article
- Cardioprotection strategies for anthracycline cardiotoxicity.Basic research in cardiology · 2025Review
- Anthracycline-Induced Cardiomyopathy in Cancer Survivors: Management and Long-Term Implications.Advances in experimental medicine and biology · 2025Review
- Natural Products From Traditional Chinese Medicine: Potential Therapeutic Agents in Cancer Therapy-Induced Cardiotoxicity.Drug design, development and therapy · 2025Review
- Epidemiology, risk factors and mechanism of breast cancer and atrial fibrillation.Cardio-oncology (London, England) · 2024Review
- Differential Expression of Circulating miRNAs and Carfilzomib-Related Cardiovascular Adverse Events in Patients with Multiple Myeloma.International journal of molecular sciences · 2024Article
- Social Determinants of Health in Cardio-Oncology: Multi-Level Strategies to Overcome Disparities in Care:JACC. CardioOncology · 2024Review
- The dual role of ferroptosis in anthracycline-based chemotherapy includes reducing resistance and increasing toxicity.Cell death discovery · 2023Review
- Evolving field of cardio-oncology.Cancer pathogenesis and therapy · 2023Review
- Exploration of the amino acid metabolic signature in anthracycline-induced cardiotoxicity using an optimized targeted metabolomics approach based on UPLC-MS/MS.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- microRNAs signatures as potential biomarkers of structural cardiotoxicity in human-induced pluripotent stem-cell derived cardiomyocytes.Archives of toxicology · 2022Article
- Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation.Pharmaceutics · 2022Review
- Impact of novel microbial secondary metabolites on the pharma industry.Applied microbiology and biotechnology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advances in cancer treatment have significantly improved the survival of patients with cancer, but, unfortunately, many of these treatments also have long-term complications. Cancer treatment-related cardiotoxicities are becoming a significant clinical problem that a new discipline, Cardio-Oncology, was established to advance the cardiovascular care of patients with growing cancer populations. Anthracyclines are a class of chemotherapeutic agents used to treat many cancers in adults and children. Their clinical use is limited by anthracycline-induced cardiotoxicity (AIC), which can lead to heart failure. Early-onset cardiotoxicity appears within a year of treatment, whereas late-onset cardiotoxicity occurs > 1 year and even up to decades after treatment completion. The pathophysiology of AIC was hypothesized to be caused by generation of reactive oxygen species that lead to lipid peroxidation, defective mitochondrial biogenesis, and DNA damage of the cardiomyocytes. The accumulation of anthracycline metabolites was also proposed to cause mitochondrial damage and the induction of cardiac cell apoptosis, which induces arrhythmias, contractile dysfunction, and cardiomyocyte death. This paper will provide a general overview of cardiotoxicity focusing on the effect of anthracyclines and their epigenetic molecular mechanisms on cardiotoxicity.
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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.