ArticleCardiovascular therapeutics2013
The effects of aging on apoptosis following myocardial infarction.
Article in Cardiovascular therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- 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
- Caspase-1 in cancer and inflammatory diseases: a potential therapeutic target.Apoptosis : an international journal on programmed cell death · 2026Review
- Emerging Gene Therapy Based on Nanocarriers: A Promising Therapeutic Alternative for Cardiovascular Diseases and a Novel Strategy in Valvular Heart Disease.International journal of molecular sciences · 2025Review
- Comprehensive analysis of aging-related genes and immune infiltration landscape in ischemic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- Impact of age and sex on myelopoiesis and inflammation during myocardial infarction.Journal of molecular and cellular cardiology · 2024Review
- Myocardial injury and clinical outcome in octogenarians after non-ST-elevation myocardial infarction.Frontiers in cardiovascular medicine · 2024Article
- Article
- Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction.Scientific reports · 2023Article
- Deoxynivalenol induces caspase-3/GSDME-dependent pyroptosis and inflammation in mouse liver and HepaRG cells.Archives of toxicology · 2022Article
- Nanocarrier-Based Targeted Therapies for Myocardial Infarction.Pharmaceutics · 2022Review
- Therapeutic Potential of Senolytics in Cardiovascular Disease.Cardiovascular drugs and therapy · 2022Review
- Senescence and senolytics in cardiovascular disease: Promise and potential pitfalls.Mechanisms of ageing and development · 2021Review
- The Role of Pathological Aging in Cardiac and Pulmonary Fibrosis.Aging and disease · 2019Article
- Novel role of extracellular matrix protein 1 (ECM1) in cardiac aging and myocardial infarction.PloS one · 2019Article
- The Dual Role of Inducible Nitric Oxide Synthase in Myocardial Ischemia/Reperfusion Injury: Friend or Foe?Oxidative medicine and cellular longevity · 2018Review
- Aging is protective against pressure overload cardiomyopathy via adaptive extracellular matrix remodeling.American journal of cardiovascular disease · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAging is associated with higher incidence of heart failure and death following myocardial infarction (MI). The molecular and cellular changes that lead to these worse outcomes are not known. METHODS AND
resultsYoung and aging mice underwent induction of MI by LAD ligation. There was a significant increase in mortality in the aging mice. Neither the young nor aging hearts after MI had inducible ventricular tachycardia. Cardiomyocyte apoptosis increases early after MI in young and aging mice, but to a much greater degree in the aging mice. Caspase inhibition with Ac-DEVD-CHO resulted in a 61% reduction in activated caspase-3 and an 84% reduction in apoptosis in cardiomyocytes in young mice (P < 0.05), but not in aging mice. Gene pathway profiling demonstrated activation of both the caspase and Map3k1/Mapk10 pathways in aging mice following MI, which may contribute to their resistance to caspase inhibition.
conclusionsAging hearts activate distinct apoptotic pathways have more cardiomyocyte apoptosis and are resistant to antiapoptotic therapies following MI. Novel or combination approaches may be required to improve outcomes in aging patients following MI.
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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.