ArticleAmerican journal of physiology. Heart and circulatory physiology2018
Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing after myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- HSP90 Inhibition Disrupts 27-Hydroxycholesterol-Induced Inflammatory Signaling in Monocytic Cells.International journal of molecular sciences · 2025Article
- The interplay of senescence and MMPs in myocardial infarction: implications for cardiac aging and therapeutics.Biogerontology · 2025Review
- Guidelines on antibody use in physiology research.American journal of physiology. Renal physiology · 2024Article
- Immunomodulation by glucocorticoid-induced leucine zipper in macrophages: enhanced phagocytosis, protection from pyroptosis, and altered mitochondrial function.Frontiers in immunology · 2024Article
- Association of troponin I and macrophages in cardiac tamponade with Stanford type A aortic dissection.Heliyon · 2023Article
- Impaired angiogenesis in ageing: the central role of the extracellular matrix.Journal of translational medicine · 2023Review
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Immunosenescence: A Critical Factor Associated With Organ Injury After Sepsis.Frontiers in immunology · 2022Review
- Mechanisms and strategies for a therapeutic cardiac immune response.Journal of molecular and cellular cardiology · 2021Article
- Article
- Infarct in the Heart: What's MMP-9 Got to Do with It?Biomolecules · 2021Review
- Network Analysis Reveals a Distinct Axis of Macrophage Activation in Response to Conflicting Inflammatory Cues.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Investigation of association of genetic variant rs3918242 of matrix metalloproteinase-9 with hypertension, myocardial infarction and progression of ventricular dysfunction in Irish Caucasian patients with diabetes: a report from the STOP-HF follow-up programme.BMC cardiovascular disorders · 2021Article
- Fibroblast contributions to ischemic cardiac remodeling.Cellular signalling · 2021Review
- Adding insult to injury - Inflammation at the heart of cardiac fibrosis.Cellular signalling · 2021Review
- Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021Review
- Proteomic assessment of serum biomarkers of longevity in older men.Aging cell · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Matrix metalloproteinase (MMP)-9 increases in the myocardium with advanced age and after myocardial infarction (MI). Because young transgenic (TG) mice overexpressing human MMP-9 only in macrophages show better outcomes post-MI, whereas aged TG mice show a worse aging phenotype, we wanted to evaluate the effect of aging superimposed on MI to see if the detrimental effect of aging counteracted the benefits of macrophage MMP-9 overexpression. We used 17- to 28-mo-old male and female C57BL/6J wild-type (WT) and TG mice ( n = 10-21 mice/group) to evaluate the effects of aging superimposed on MI. Despite similar infarct areas and mortality rates at day 7 post-MI, aging TG mice showed improved diastolic properties and remodeling index compared with WT mice (both P < 0.05). Macrophage numbers were higher in TG than WT mice at days 0 and 7 post-MI, and the post-MI increase was due to elevated cluster of differentiation 18 protein levels (all P < 0.05). RNA sequencing analysis of cardiac macrophages isolated from day 7 post-MI infarcts identified 1,276 statistically different (all P < 0.05) genes (994 increased and 282 decreased in TG mice). Reduced expression of vascular endothelial growth factor A, platelet-derived growth factor subunit A, and transforming growth factor-β
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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.