ReviewJournal of molecular medicine (Berlin, Germany)2017
Doxorubicin-induced chronic dilated cardiomyopathy-the apoptosis hypothesis revisited.
Review in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed.
- Apelin-13 attenuates doxorubicin-induced myocardial injury via the PI3K/AKT and ERK/MAPK signaling pathways.Cardiovascular diagnosis and therapy · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- The Effects of Salicyluric Acid, the Main Metabolite of Aspirin, on Lipid Peroxidation Induced by Iron and Copper Ions in a Lipid Membrane Model.International journal of molecular sciences · 2026Article
- Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Doxorubicin or Epirubicin Versus Liposomal Doxorubicin Therapy-Differences in Cardiotoxicity.Cardiovascular toxicology · 2025Review
- Novel Anthraquinone Derivatives and Their Complexes with Metal Ions with Anticancer Activity: Structure/Redox and Chelation Activity Correlations.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Cytotoxic and ROS generation activity of anthraquinones chelate complexes with metal ions.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Article
- Knockdown of HDAC6 alleviates ventricular remodeling in experimental dilated cardiomyopathy via inhibition of NLRP3 inflammasome activation and promotion of cardiomyocyte autophagy.Cell biology and toxicology · 2023Article
- Increased Free Radical Generation during the Interaction of a Quinone-Quinoline Chelator with Metal Ions and the Enhancing Effect of Light.Pharmaceuticals (Basel, Switzerland) · 2023Article
- The Interaction of Anthracycline Based Quinone-Chelators with Model Lipid Membranes:Membranes · 2023Article
- CD47 antibody protects mice from doxorubicin-induced myocardial damage by suppressing cardiomyocyte apoptosis.Experimental and therapeutic medicine · 2022Article
- The Interplay of Ascorbic Acid with Quinones-Chelators-Influence on Lipid Peroxidation: Insight into Anticancer Activity.Antioxidants (Basel, Switzerland) · 2022Article
- Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- I-κB kinase-ε deficiency improves doxorubicin-induced dilated cardiomyopathy by inhibiting the NF-κB pathway.Frontiers in physiology · 2022Article
- Identification of novel biomarkers involved in doxorubicin-induced acute and chronic cardiotoxicity, respectively, by integrated bioinformatics.Frontiers in cardiovascular medicine · 2022Article
- Periplocymarin Alleviates Doxorubicin-Induced Heart Failure and Excessive Accumulation of Ceramides.Frontiers in cardiovascular medicine · 2021Article
- High expression levels and localization of Sox5 in dilated cardiomyopathy.Molecular medicine reports · 2020Article
- Toll-like receptor 5 deficiency diminishes doxorubicin-induced acute cardiotoxicity in mice.Theranostics · 2020Article
- Peroxiredoxin-1 Overexpression Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and Cardiomyocyte Apoptosis.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chemotherapeutic agent doxorubicin (DOX) has significantly increased survival rates of pediatric and adult cancer patients. However, 10% of pediatric cancer survivors will 10-20 years later develop severe dilated cardiomyopathy (DCM), whereby the exact molecular mechanisms of disease progression after this long latency time remain puzzling. We here revisit the hypothesis that elevated apoptosis signaling or its increased likelihood after DOX exposure can lead to an impairment of cardiac function and cause a cardiac dilation. Based on recent literature evidence, we first argue why a dilated phenotype can occur when little apoptosis is detected. We then review findings suggesting that mature cardiomyocytes are protected against DOX-induced apoptosis downstream, but not upstream of mitochondrial outer membrane permeabilisation (MOMP). This lack of MOMP induction is proposed to alter the metabolic phenotype, induce hypertrophic remodeling, and lead to functional cardiac impairment even in the absence of cardiomyocyte apoptosis. We discuss findings that DOX exposure can lead to increased sensitivity to further cardiomyocyte apoptosis, which may cause a gradual loss in cardiomyocytes over time and a compensatory hypertrophic remodeling after treatment, potentially explaining the long lag time in disease onset. We finally note similarities between DOX-exposed cardiomyocytes and apoptosis-primed cancer cells and propose computational system biology as a tool to predict patient individual DOX doses. In conclusion, combining recent findings in rodent hearts and cardiomyocytes exposed to DOX with insights from apoptosis signal transduction allowed us to obtain a molecularly deeper insight in this delayed and still enigmatic pathology of DCM.
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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.