ReviewToxics2025
Pathophysiology of Doxorubicin-Mediated Cardiotoxicity.
Review in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Article
- Doxorubicin-Induced Cytotoxicity in Adipose-Derived Stem Cells Is Associated With Altered SAPK/JNK Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cardiovascular Protection with Sulfasalazine During Doxorubicin Challenge: Evidence from Oxidative and Histologic Endpoints.Biomolecules · 2026Article
- Review
- Identification of TGF-β1 as a key regulator in DOX-induced cardiotoxicity.Journal of cardiothoracic surgery · 2026Article
- Oxidative DNA Damage as an Integrative Marker of Redox Dysfunction Associated with Doxorubicin-Induced Cardiotoxicity in Pediatric Leukemia.Current issues in molecular biology · 2026Article
- Disphosphate based hydrogel microspheres for targeted transarterial radioembolization and chemoembolization therapies.Journal of advanced research · 2026Article
- Evaluation of vinpocetine in an acute doxorubicin-induced cardiotoxicity model in rats.Scientific reports · 2026Article
- Article
- RNAi-mediated p38δ silencing mitigates anthracycline cardiotoxicity in female mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Ginkgetin Alleviates Doxorubicin-Induced Heart Failure by Regulating Mitochondrial Dysfunction Through the AMPK/Sirt1/NF-κB Signaling Pathway.Balkan medical journal · 2026Article
- Synergistic therapeutic impact of dichloroacetate nanoparticles and doxorubicin in modulating pyruvate dehydrogenase kinase in breast carcinoma model.Scientific reports · 2026Article
- GLP-1 Receptor Agonist Exenatide Protects Against Doxorubicin-Induced Cardiotoxicity Through the SIRT1 Pathway: An Electrocardiographic, 99mTc-PYP Scintigraphic, and Biochemical Study.Medicina (Kaunas, Lithuania) · 2026Article
- Hyperoside Inhibits Doxorubicin-Induced Ferroptosis in Cardiomyocytes via the Nrf2/GPX4 Pathway.Journal of cardiovascular translational research · 2026Article
- Doxorubicin-induced cardiotoxicity: Is ferroptosis the primary driver or a downstream amplifier?EXCLI journal · 2026Review
- Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review.Drug design, development and therapy · 2026Review
- Lycorine Attenuates Cardiac Fibrosis Through the Regulation of PYK2 Expression and Activity.Cardiovascular therapeutics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is used for the treatment of various malignancies, including leukemias, lymphomas, sarcomas, and bladder, breast, and gynecological cancers in adults, adolescents, and children. However, DOX causes severe side effects in patients, such as cardiotoxicity, which encompasses heart failure, arrhythmia, and myocardial infarction. DOX-induced cardiotoxicity (DIC) is based on the combination of nuclear-mediated cardiomyocyte death and mitochondrial-mediated death. Oxidative stress, altered autophagy, inflammation, and apoptosis/ferroptosis represent the main pathogenetic mechanisms responsible for DIC. In addition, in vitro and in vivo models of DIC sirtuins (SIRT), and especially, SIRT 1 are reduced, and this event contributes to cardiac damage. In fact, SIRT 1 inhibits reactive oxygen species and NF-kB activation, thus improving myocardial oxidative stress and cardiac remodeling. Therefore, the recovery of SIRT 1 during DIC may represent a therapeutic strategy to limit DIC progression. Natural products, i.e., polyphenols, as well as nano formulations of DOX and iron chelators, are other potential compounds experimented with in models of DIC. At present, few clinical trials are available to confirm the efficacy of these products in DIC. The aim of this review is the description of the pathophysiology of DIC as well as potential drug targets to alleviate DIC.
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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.