ArticleThe Journal of clinical investigation2005
Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.
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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
135 citing papers in PubMed, 322 citations in OpenAlex.
- Association of polymorphisms of zinc metalloproteinases with clinical response to stem cell therapy.Herz · 2010Trial
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- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Matrix metalloproteinases and risk of cardiovascular mortality and morbidity in the United Kingdom: A prospective cohort study with machine learning analysis.Preventive medicine reports · 2026Article
- Integrative Transcriptomic-Histological Analysis in Dilated Cardiomyopathy Unveils FGFR1 Inhibition as Anti-Cardiac Fibrotic and Cardioprotective Therapy.JACC. Basic to translational science · 2025Article
- The cGAS-STING pathway promotes acute ischemia-induced neutropoiesis and neutrophil priming in the bone marrow.Basic research in cardiology · 2025Article
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- Matrix Metalloproteinases: Pathophysiologic Implications and Potential Therapeutic Targets in Cardiovascular Disease.Biomolecules · 2025Review
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- Hitting the Target! Challenges and Opportunities for TGF-β Inhibition for the Treatment of Cardiac fibrosis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Cardiomyocyte Alpha-1A Adrenergic Receptors Mitigate Postinfarct Remodeling and Mortality by Constraining Necroptosis.JACC. Basic to translational science · 2024Article
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Progranulin deficiency exacerbates cardiac remodeling after myocardial infarction.FASEB bioAdvances · 2023Article
- Loss of Bone Morphogenetic Protein-9 Reduces Survival and Increases MMP Activity After Myocardial Infarction.JACC. Basic to translational science · 2023Article
- Review
- Association between MMP2 gene polymorphisms and dilated cardiomyopathy in a Chinese Han population.ESC heart failure · 2023Article
- Matrix metalloproteinases in coronary artery disease and myocardial infarction.Basic research in cardiology · 2023Review
- Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation.Frontiers in immunology · 2023Review
- Molecular Background of Toxic-Substances-Induced Morphological Alterations in the Umbilical Cord Vessels and Fetal Red Blood Cells.International journal of molecular sciences · 2022Article
- Matrix Metalloproteinase 2 as a Pharmacological Target in Heart Failure.Pharmaceuticals (Basel, Switzerland) · 2022Review
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MMPs are implicated in LV remodeling after acute myocardial infarction (MI). To analyze the role of MMP-2, we generated MI by ligating the left coronary artery of MMP-2-KO and WT mice, the latter of which were administered orally an MMP-2-selective inhibitor or vehicle (TISAM). The survival rate was significantly higher in MMP-2-KO and TISAM-treated mice than in control WT mice. The main cause of mortality in control WT mice was cardiac rupture, which was not observed in MMP-2-KO or TISAM-treated mice. Control WT mice, but not MMP-2-KO or TISAM-treated mice, showed activation of the zymogen of MMP-2, strong gelatinolytic activity, and degradation of ECM components, including laminin and fibronectin, in the infarcted myocardium. Although infarcted cardiomyocytes in control WT mice were rapidly removed by macrophages, the removal was suppressed in MMP-2-KO and TISAM-treated mice. Macrophage migration was induced by the infarcted myocardial tissue from control WT mice and was inhibited by treatment of macrophages with laminin or fibronectin peptides prior to migration assay. These data suggest that inhibition of MMP-2 activity improves the survival rate after acute MI by preventing cardiac rupture and delays post-MI remodeling through a reduction in macrophage infiltration.
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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.