ArticleAging cell2020
Clearance of senescent cells during cardiac ischemia-reperfusion injury improves recovery.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07693712 (Coronary Artery Bypass Surgery After Myocardial Infarction), which is not on this map. Cited by 122 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.
Coronary Artery Bypass Surgery After Myocardial Infarction: Identifying Clinical Outcomes by Analysing the Senescence Associated Secretory Phenotype
Who cites it
122 citing papers in PubMed, 163 citations in OpenAlex.
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Targeting ACTG1 alleviates isoproterenol-induced cardiac injury by regulating endothelial-to-mesenchymal transition.Journal of molecular histology · 2026Article
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Epicardial Contributions to Fibro-Inflammatory Signaling in a Pkp2-Deficient Arrhythmogenic Cardiomyopathy Model.Circulation. Heart failure · 2026Article
- Review
- Isoproterenol Induces Cardiac Injury and Senescence in Sprague-Dawley Rats: A Cost-Effective Pharmacological Model.Biomedicines · 2026Article
- Synergistic senolytic-regenerative therapy significantly extends healthspan and lifespan.Journal of translational medicine · 2026Article
- Triple-Marker Screening of 20 Terpenes Identifies Candidate Modulators of Senescence-Associated Phenotypes in D-Galactose-Treated Endothelial Cells.Molecules (Basel, Switzerland) · 2026Article
- CK1-induced TERT phosphorylation mediates mitochondrial translocation to inhibit cardiomyocyte senescence and alleviate myocardial ischemia-reperfusion injury.Cell biology and toxicology · 2026Article
- Exercise-Induced Exerkines Modulate Autophagy: Implications for Interorgan Crosstalk in the Hallmarks of Ageing.International journal of molecular sciences · 2026Review
- Glycative Stress Disrupts the Mitochondrial-Lysosome Axis and Promotes Geroconversion in Aging Cardiomyocytes.Aging cell · 2026Article
- Interconnected Pathways and Therapeutic Implications for Cardiovascular Aging and Diseases.JACC. Asia · 2026Review
- The role of cellular senescence-related genes in ischemia-reperfusion injury and the identification of their biomarkers.Scientific reports · 2026Article
- iRhom2 regulates HMGB1 secretion to modulate inflammation and hepatocyte senescence in an in vitro model of ischemia-reperfusion injury.Cell death & disease · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Integrating senotherapeutics into transplantation: liver reconditioning in an aging donor pool.Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- (Pro)renin receptor promotes cardiomyocyte senescence via tripartite motif-containing 24-mediated stabilization of p53 in diabetic cardiomyopathy.Acta biochimica et biophysica Sinica · 2025Article
- The promise of organ rejuvenation to overcome the shortage in organ transplantation.Nature communications · 2025Review
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 5 institutions in 4 countries.
Funding
Abstract
A key component of cardiac ischemia-reperfusion injury (IRI) is the increased generation of reactive oxygen species, leading to enhanced inflammation and tissue dysfunction in patients following intervention for myocardial infarction. In this study, we hypothesized that oxidative stress, due to ischemia-reperfusion, induces senescence which contributes to the pathophysiology of cardiac IRI. We demonstrate that IRI induces cellular senescence in both cardiomyocytes and interstitial cell populations and treatment with the senolytic drug navitoclax after ischemia-reperfusion improves left ventricular function, increases myocardial vascularization, and decreases scar size. SWATH-MS-based proteomics revealed that biological processes associated with fibrosis and inflammation that were increased following ischemia-reperfusion were attenuated upon senescent cell clearance. Furthermore, navitoclax treatment reduced the expression of pro-inflammatory, profibrotic, and anti-angiogenic cytokines, including interferon gamma-induced protein-10, TGF-β3, interleukin-11, interleukin-16, and fractalkine. Our study provides proof-of-concept evidence that cellular senescence contributes to impaired heart function and adverse remodeling following cardiac ischemia-reperfusion. We also establish that post-IRI the SASP plays a considerable role in the inflammatory response. Subsequently, senolytic treatment, at a clinically feasible time-point, attenuates multiple components of this response and improves clinically important parameters. Thus, cellular senescence represents a potential novel therapeutic avenue to improve patient outcomes following cardiac ischemia-reperfusion.
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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.