ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2016
Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 4 of them syntheses that pooled it.
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Who cites it
51 citing papers in PubMed, 4 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- Potential role of a three-gene signature in predicting diagnosis in patients with myocardial infarction.Bioengineered · 2021Pooled it
- 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
- Guidelines for measuring cardiac physiology in mice.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
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Associations of inflammatory biomarkers with clinical outcomes in degenerative lumbar spinal stenosis: A systematic review.Brain & spine · 2026Review
- The role and therapeutic advances of neutrophils in acute myocardial infarction: from traditional chinese medicine modulation to modern therapeutic strategies.Chinese medicine · 2025Review
- Multi-Omic Associations of Epigenetic Age Acceleration Are Heterogeneously Shaped by Genetic and Environmental Influences.Aging cell · 2025Article
- The interplay of senescence and MMPs in myocardial infarction: implications for cardiac aging and therapeutics.Biogerontology · 2025Review
- Deleting fibroblast growth factor 2 in macrophages aggravates septic acute lung injury by increasing M1 polarization and inflammatory cytokine secretion.Molecular biomedicine · 2024Article
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- Article
- Brain-Derived Neurotrophic Factor Precursor Contributes to a Proinflammatory Program in Monocytes/Macrophages After Acute Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation.Frontiers in immunology · 2023Review
- Neutrophil degranulation and myocardial infarction.Cell communication and signaling : CCS · 2022Review
- Identification and validation of senescence-related genes in circulating endothelial cells of patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
- Single-Cell Sequencing Revealed Pivotal Genes Related to Prognosis of Myocardial Infarction Patients.Computational and mathematical methods in medicine · 2022Article
- Phosphodiesterase-5a Knock-out Suppresses Inflammation by Down-Regulating Adhesion Molecules in Cardiac Rupture Following Myocardial Infarction.Journal of cardiovascular translational research · 2021Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
In this study, we examined the combined effect of aging and myocardial infarction on left ventricular remodeling, focusing on matrix metalloproteinase (MMP)-9-dependent mechanisms. We enrolled 55 C57BL/6J wild type (WT) and 85 MMP-9 Null (Null) mice of both sexes at 11-36 months of age and evaluated their response at Day 7 post-myocardial infarction. Plasma MMP-9 levels positively linked to age in WT mice (r = .46, p = .001). MMP-9 deletion improved survival (76% for WT vs 88% for Null, p = .021). Post-myocardial infarction, there was a progressive increase in left ventricular dilation with age in WT but not in Null mice. By inflammatory gene array analysis, WT mice showed linear age-dependent increases in three different proinflammatory genes (C3, CCl4, and CX3CL1; all p < .05), whereas Null mice showed increases in three proinflammatory genes (CCL5, CCL9, and CXCL4; all p < .05) and seven anti-inflammatory genes (CCL1, CCL6, CCR1, IL11, IL1r2, IL8rb, and Mif; all p < .05). Compared with WT, macrophages isolated from Null left ventricle infarct demonstrated enhanced expression of anti-inflammatory M2 markers CD163, MRC1, TGF-β1, and YM1 (all p < .05), without affecting proinflammatory M1 markers. In conclusion, MMP-9 deletion stimulated anti-inflammatory polarization of macrophages to attenuate left ventricle dysfunction in the aging post-myocardial infarction.
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Registered trials
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