ArticleAging cell2019
Pharmacological clearance of senescent cells improves survival and recovery in aged mice following acute myocardial infarction.
Article in Aging cell, 2019. 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 153 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
153 citing papers in PubMed, 232 citations in OpenAlex.
- Activation of telomerase by TA-65 enhances immunity and reduces inflammation post myocardial infarction.GeroScience · 2023Trial
- Harnessing the NKG2D immune surveillance pathway using engineered T-cells for the treatment of human disease.Human vaccines & immunotherapeutics · 2026Review
- Young Mice Exhibit Increased Relative Ventricular Remodeling After AMI-A Longitudinal CMR Study.Aging cell · 2026Article
- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
- Article
- Cellular senescence and inflammageing: from mechanisms to senotherapeutic interventions.Biogerontology · 2026Review
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Review
- Isoproterenol Induces Cardiac Injury and Senescence in Sprague-Dawley Rats: A Cost-Effective Pharmacological Model.Biomedicines · 2026Article
- Aging diminishes thymic output, reduces naive T cells, promotes memory T-cell accumulation, and impairs thymic regeneration.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Review
- The Senolytic Drug Navitoclax Protects the Brain After Experimental Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Jinxinkang Granule Preserves Myocardial Function by Suppressing Cardiac Senescence Through the cGAS-STING Axis in a Pressure Overload Mouse Model of Heart Failure.Cardiovascular toxicology · 2026Article
- Glycative Stress Disrupts the Mitochondrial-Lysosome Axis and Promotes Geroconversion in Aging Cardiomyocytes.Aging cell · 2026Article
- Targeting senescent cells in aged adipose tissue induced by ovarian cancer with the NF-κB inhibitor quercetin and resveratrol impedes the growth and metastasis of ovarian cancer.Science China. Life sciences · 2026Article
- Translating cellular senescence research into clinical practice for metabolic disease.Nature reviews. Endocrinology · 2026Review
- The role of cellular senescence-related genes in ischemia-reperfusion injury and the identification of their biomarkers.Scientific reports · 2026Article
- Cellular Senescence in the Ascending Aorta and Complexity of Coronary Atherosclerosis.Journal of aging research · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
93 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
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiovascular disease is the leading cause of death in individuals over 60 years old. Aging is associated with an increased prevalence of coronary artery disease and a poorer prognosis following acute myocardial infarction (MI). With age, senescent cells accumulate in tissues, including the heart, and contribute to age-related pathologies. However, the role of senescence in recovery following MI has not been investigated. In this study, we demonstrate that treatment of aged mice with the senolytic drug, navitoclax, eliminates senescent cardiomyocytes and attenuates profibrotic protein expression in aged mice. Importantly, clearance of senescent cells improved myocardial remodelling and diastolic function as well as overall survival following MI. These data provide proof-of-concept evidence that senescent cells are major contributors to impaired function and increased mortality following MI and that senolytics are a potential new therapeutic avenue for MI.
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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.