ArticleJournal of the American Heart Association2016
Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- A Systematic Review of the Potential Chemoprotective Effects of Resveratrol on Doxorubicin-Induced Cardiotoxicity: Focus on the Antioxidant, Antiapoptotic, and Anti-Inflammatory Activities.Oxidative medicine and cellular longevity · 2021Pooled it
- CHK1 activates mitophagy to attenuate cardiac aging via inhibiting AHSA1-ubiquitination.Redox biology · 2026Article
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- P2Y12-AMPKα2 signaling contributes to cardiomyocyte senescence in doxorubicin-induced heart failure.Molecular and cellular biochemistry · 2026Article
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence.Biology · 2026Article
- Isoproterenol Induces Cardiac Injury and Senescence in Sprague-Dawley Rats: A Cost-Effective Pharmacological Model.Biomedicines · 2026Article
- Development of Magnetic Microbeads Equipped with Temperature-Responsive Artificial Antibodies for Efficient Anticancer Drug Administration.Analytical chemistry · 2026Article
- Myocardial testosterone glucuronide and disease phenotypes in hypertrophic cardiomyopathy.ESC heart failure · 2026Article
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- A Comprehensive Multiomics Signature of Doxorubicin-Induced Cellular Senescence in the Postmenopausal Human Ovary.Aging cell · 2025Article
- Cancer therapy-related cardiovascular aging: mechanisms, monitoring, and intervention strategies.Frontiers in cardiovascular medicine · 2025Review
- A comprehensive review on the effects of sex hormones on chemotherapy-induced cardiotoxicity: are they lucrative or unprofitable?Cardio-oncology (London, England) · 2024Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- Pediatric Cardio-Oncology: Screening, Risk Stratification, and Prevention of Cardiotoxicity Associated with Anthracyclines.Children (Basel, Switzerland) · 2024Review
- Exosomal miR-9-5p derived from iPSC-MSCs ameliorates doxorubicin-induced cardiomyopathy by inhibiting cardiomyocyte senescence.Journal of nanobiotechnology · 2024Article
- Priorities in Cardio-Oncology Basic and Translational Science: GCOS 2023 Symposium Proceedings:JACC. CardioOncology · 2023Review
- Article
- Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity.Reviews in cardiovascular medicine · 2023Review
- Sex, aging, immunity and adrenal cancer.Nature aging · 2023Article
- Therapeutic opportunities for senolysis in cardiovascular disease.The FEBS journal · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic cardiotoxicity is less common in male than in female patients receiving doxorubicin and other anthracyclines at puberty and adolescence. We hypothesized that this sex difference might be secondary to distinct activities of sex hormones on cardiomyocyte senescence, which is thought to be central to the development of long-term anthracycline cardiomyopathy. METHODS AND
resultsH9c2 cells and neonatal mouse cardiomyocytes were exposed to doxorubicin with or without prior incubation with testosterone or 17β-estradiol, the main androgen and estrogen, respectively. Testosterone, but not 17β-estradiol, counteracted doxorubicin-elicited senescence. Downregulation of telomere binding factor 2, which has been pinpointed previously as being pivotal to doxorubicin-induced senescence, was also prevented by testosterone, as were p53 phosphorylation and accumulation. Pretreatment with the androgen receptor antagonist flutamide, the phosphatidylinositol 3 kinase inhibitor LY294002, and the nitric oxide synthase inhibitor L-NG-nitroarginine methyl ester abrogated the reduction in senescence and the normalization of telomere binding factor 2 levels attained by testosterone. Consistently, testosterone enhanced the phosphorylation of AKT and nitric oxide synthase 3. In H9c2 cells, doxorubicin-stimulated senescence was still observed up to 21 days after treatment and increased further when cells were rechallenged with doxorubicin 14 days after the first exposure to mimic the schedule of anthracycline-containing chemotherapy. Remarkably, these effects were also inhibited by testosterone.
conclusionsTestosterone protects cardiomyocytes against senescence caused by doxorubicin at least in part by modulating telomere binding factor 2 via a pathway involving the androgen receptor, phosphatidylinositol 3 kinase, AKT, and nitric oxide synthase 3. This is a potential mechanism by which pubescent and adolescent boys are less prone to chronic anthracycline cardiotoxicity than girls.
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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.