ReviewFrontiers in cell and developmental biology2023
Cell death regulation in myocardial toxicity induced by antineoplastic drugs.
Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Quercetin Activates NRF2/SLC7A11/GPX4 Signaling to Restore Mitochondrial Function Inhibit Ferroptosis Thereby Alleviating Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2026Article
- VSNL1 attenuates hypoxia‑induced myocardial apoptosis by regulating the CNP/NPRB pathway.Molecular medicine reports · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Ferroptosis regulation in doxorubicin-induced cardiotoxicity: multi-mechanism interventions and translational strategies.Frontiers in pharmacology · 2026Review
- Review
- Entrectinib binds to HMGB1 and activates cardiomyocyte autophagy by inhibiting OTUD5-MTORC1 signaling to induce cardiotoxicity.Autophagy · 2025Article
- Review
- NEDD4L-Mediated Ubiquitination of GPX4 Exacerbates Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Article
- Lipid Metabolism Reprogramming in Cancer: Insights into Tumor Cells and Immune Cells Within the Tumor Microenvironment.Biomedicines · 2025Review
- Roles of Autophagy, Mitophagy, and Mitochondria in Left Ventricular Remodeling after Myocardial Infarction.Reviews in cardiovascular medicine · 2025Review
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- Indole-3-Lactic Acid Inhibits Doxorubicin-Induced Ferroptosis Through Activating Aryl Hydrocarbon Receptor/Nrf2 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Fasting: A Complex, Double-Edged Blade in the Battle Against Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2024Review
- The Current State of Realistic Heart Models for Disease Modelling and Cardiotoxicity.International journal of molecular sciences · 2024Review
- Anthracycline cardiotoxicity is exacerbated by global p38β genetic ablation in a sexually dimorphic manner but unaltered by cardiomyocyte-specific p38α loss.American journal of physiology. Heart and circulatory physiology · 2023Article
- The dual role of ferroptosis in anthracycline-based chemotherapy includes reducing resistance and increasing toxicity.Cell death discovery · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homeostatic regulation of cardiomyocytes plays a critical role in maintaining normal physiological activity of cardiac tissue. Severe cardiotoxicity can lead to heart disease, including but not limited to arrhythmias, myocardial infarction and cardiac hypertrophy. In recent years, significant progress has been made in developing new therapies for cancer that have dramatically changed the treatment of several malignancies and continue to improve patient survival, but can also lead to serious cardiac adverse effects. Mitochondria are key organelles that maintain homeostasis in myocardial tissue and have been extensively involved in various cardiovascular disease episodes, including ischemic cardiomyopathy, heart failure and stroke. Several studies support that mitochondrial targeting is a major determinant of the cardiotoxic effects triggered by chemotherapeutic agents increasingly used in solid and hematologic tumors. This antineoplastic therapy-induced mitochondrial toxicity is due to different mechanisms, usually altering the mitochondrial respiratory chain, energy production and mitochondrial kinetics, or inducing mitochondrial oxidative/nitrosative stress, ultimately leading to cell death. This review focuses on recent advances in forms of cardiac cell death and related mechanisms of antineoplastic drug-induced cardiotoxicity, including autophagy, ferroptosis, apoptosis, pyroptosis, and necroptosis, explores and evaluates key proteins involved in cardiac cell death signaling, and presents recent advances in cardioprotective strategies for this disease. It aims to provide theoretical basis and targets for the prevention and treatment of pharmacological cardiotoxicity in clinical settings.
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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.