ArticleJournal of the American College of Cardiology2008
Aging-related defects are associated with adverse cardiac remodeling in a mouse model of reperfused myocardial infarction.
Article in Journal of the American College of Cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 2 of them syntheses that pooled it.
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Who cites it
117 citing papers in PubMed, 2 syntheses or guidelines pooled it, 192 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Young Mice Exhibit Increased Relative Ventricular Remodeling After AMI-A Longitudinal CMR Study.Aging cell · 2026Article
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Age-dependent dysregulation of collagen metabolism in primary cardiac fibroblasts in vitro.Cardiovascular research · 2026Article
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment.European heart journal · 2026Review
- Cellular senescence and cell therapy in cardiovascular diseases.Stem cell research & therapy · 2025Review
- Article
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Comparison of Myocardial Function in Young and Old Mice During Acute Myocardial Infarction: A Cardiac Magnetic Resonance Study.Diagnostics (Basel, Switzerland) · 2025Article
- Clinical benefits of evolocumab in diabetic patients with STEMI undergoing PCI: a retrospective study.American journal of translational research · 2025Article
- Role of NLRP3 Inflammasome in Heart Failure Patients Undergoing Cardiac Surgery as a Potential Determinant of Postoperative Atrial Fibrillation and Remodeling: Is SGLT2 Cotransporter Inhibition an Alternative for Cardioprotection?Antioxidants (Basel, Switzerland) · 2024Review
- Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- An image-driven micromechanical approach to characterize multiscale remodeling in infarcted myocardium.Acta biomaterialia · 2024Article
- An interferon gamma response signature links myocardial aging and immunosenescence.Cardiovascular research · 2023Article
- Cardiac macrophages and emerging roles for their metabolism after myocardial infarction.The Journal of clinical investigation · 2023Review
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectivesThe purpose of this study was to study aging-associated alterations in the inflammatory and reparative response after myocardial infarction (MI) and their involvement in adverse post-infarction remodeling of the senescent heart.
backgroundAdvanced age is a predictor of death and ventricular dilation in patients with MI; however, the cellular mechanisms responsible for increased remodeling of the infarcted senescent heart remain poorly understood.
methodsHistomorphometric, molecular, and echocardiographic end points were compared between young and senescent mice undergoing reperfused infarction protocols. The response of young and senescent mouse cardiac fibroblasts to transforming growth factor (TGF)-beta stimulation was examined.
resultsSenescence was associated with decreased and delayed neutrophil and macrophage infiltration, markedly reduced cytokine and chemokine expression in the infarcted myocardium, and impaired phagocytosis of dead cardiomyocytes. Reduced inflammation in senescent mouse infarcts was followed by decreased myofibroblast density and markedly diminished collagen deposition in the scar. The healing defects in senescent animals were associated with enhanced dilative and hypertrophic remodeling and worse systolic dysfunction. Fibroblasts isolated from senescent mouse hearts showed a blunted response to TGF-beta1.
conclusionsAlthough young mice exhibit a robust post-infarction inflammatory response and form dense collagenous scars, senescent mice show suppressed inflammation, delayed granulation tissue formation, and markedly reduced collagen deposition. These defects might contribute to adverse remodeling. These observations suggest that caution is necessary when attempting to therapeutically target the post-infarction inflammatory response in patients with reperfused MI. The injurious potential of inflammatory mediators might have been overstated, owing to extrapolation of experimental findings from young animals to older human patients.
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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.