ArticleThe journal of cardiovascular aging2024
Cardiomyocyte senescence and the potential therapeutic role of senolytics in the heart.
Article in The journal of cardiovascular aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Clearance of p16-positive cardiac cells improves age-related cardiac remodeling in mice.Experimental physiology · 2026Article
- Inflammaging and cytokine-driven cardiovascular senescence in age-related myocardial infarction: mechanisms, biomarkers, and precision immunotherapy strategies.Biogerontology · 2026Review
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
- Established and emerging roles of lysosomal dysfunction in cardiac aging.Nature cardiovascular research · 2026Review
- Senescence modulated cardiac repair with pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Adoptive T-cell therapies for persistent COVID-19 in immunocompromised patients: Comparison of IFN-γ virus-specific T-cell therapy and CD45RAGeroScience · 2026Article
- Inhibiting the Hif-1α-Drp1 axis alleviates mitochondrial dysfunction and reduces senescence-like changes in myocardial tissue after acute myocardial infarction.Biology direct · 2026Article
- Inhibition of PAI-1 shifts cardiomyocyte fate from senescence toward apoptosis and mitigates doxorubicin-induced cardiotoxicity.Geromedicine · 2026Article
- Gastrodin alleviates cardiomyocyte senescence by regulating autophagy through the AMPK/mTOR/4EBP1 pathway.Frontiers in pharmacology · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- Inducing Oxidative Stress-Driven Senescent Phenotype in Induced Pluripotent Stem Cell Derived Cardiomyocytes.Cell biochemistry and biophysics · 2025Article
- Role of Vascular Niche in Cardiac Aging.Circulation research · 2025Article
- S913 phosphorylation of Ulk1 protects the heart from aging through inhibition of cardiac senescence.Cardiovascular research · 2025Article
- Intersection of Cardio-Oncology: An Overview of Radiation-Induced Heart Disease in the Context of Tumors.Journal of the American Heart Association · 2025Review
- Is Senolytic Therapy in Cardiovascular Diseases Ready for Translation to Clinics?Biomolecules · 2025Review
- The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues.Frontiers in cell and developmental biology · 2025Review
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cellular senescence in cardiomyocytes, characterized by cell cycle arrest, resistance to apoptosis, and the senescence-associated secretory phenotype, occurs during aging and in response to various stresses, such as hypoxia/reoxygenation, ischemia/reperfusion, myocardial infarction (MI), pressure overload, doxorubicin treatment, angiotensin II, diabetes, and thoracic irradiation. Senescence in the heart has both beneficial and detrimental effects. Premature senescence of myofibroblasts has salutary effects during MI and pressure overload. On the other hand, persistent activation of senescence in cardiomyocytes precipitates cardiac dysfunction and adverse remodeling through paracrine mechanisms during MI, myocardial ischemia/reperfusion, aging, and doxorubicin-induced cardiomyopathy. Given the adverse roles of senescence in many conditions, specific removal of senescent cells, i.e., senolysis, is of great interest. Senolysis can be achieved using senolytic drugs (such as Navitoclax, Dasatinib, and Quercetin), pharmacogenetic approaches (including INK-ATTAC and AP20187, p16-3MR and Ganciclovir, p16 ablation, and p16-LOX-ATTAC and Cre), and immunogenetic interventions (CAR T cells or senolytic vaccination). In order to enhance the specificity and decrease the off-target effects of senolytic approaches, investigation into the mechanisms through which cardiomyocytes develop and/or maintain the senescent state is needed.
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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.