ArticleJournal of molecular and cellular cardiology2012
Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- Sodium tanshinone IIA sulfonate prevents the adverse left ventricular remodelling: Focus on polymorphonuclear neutrophil-derived granule components.Journal of cellular and molecular medicine · 2019Trial
- Dendritic Cells Derived MMP9 Fuels Sepsis-Induced Cardiac Dysfunction Through JNK/AP1 Driven Pro-Inflammatory Cytokine and Nitric Oxide Storm.Inflammation · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- The role and therapeutic advances of neutrophils in acute myocardial infarction: from traditional chinese medicine modulation to modern therapeutic strategies.Chinese medicine · 2025Review
- Single-cell RNA sequencing reveals the potential role of Postn(+) fibroblasts in promoting the progression of myocardial fibrosis after myocardial infarction.Scientific reports · 2025Article
- Matrix Metalloproteinase-9 Enhances Osteoclastogenesis: Insights from Transgenic Rabbit Bone Marrow Models and In Vitro Studies.International journal of molecular sciences · 2025Article
- Prognostic value of the neutrophil percentage-to-albumin ratio for mortality in ICU patients with myocardial infarction: a retrospective cohort and machine learning analysis.Frontiers in cardiovascular medicine · 2025Article
- Metalloproteinases (MMPs) in hypertensive disorders: role, function, pharmacology, and potential strategies to mitigate pathophysiological changes.Frontiers in pharmacology · 2025Review
- Wound healing and photoprotection properties of Acanthus ebracteatus Vahl. extracts standardized in verbascoside.Scientific reports · 2024Article
- Brain-Derived Neurotrophic Factor Precursor Contributes to a Proinflammatory Program in Monocytes/Macrophages After Acute Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Cardiovascular Biomarkers: Lessons of the Past and Prospects for the Future.International journal of molecular sciences · 2022Review
- Neutrophil degranulation and myocardial infarction.Cell communication and signaling : CCS · 2022Review
- Inflammatory cells in the ascending aortic aneurysm in patients with type 2 diabetes versus patients with hypertension.Bosnian journal of basic medical sciences · 2022Article
- Disparate effects of MMP and TIMP modulation on coronary atherosclerosis and associated myocardial fibrosis.Scientific reports · 2021Article
- 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
- Blockade of the Notch Signaling Pathway Promotes M2 Macrophage Polarization to Suppress Cardiac Fibrosis Remodeling in Mice With Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Article
- MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis.Frontiers in immunology · 2021Article
- Immune regulation of cardiac fibrosis post myocardial infarction.Cellular signalling · 2021Review
- Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction.Journal of molecular and cellular cardiology · 2020Article
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Abstract
Following myocardial infarction (MI), activated macrophages infiltrate into the necrotic myocardium as part of a robust pro-inflammatory response and secrete matrix metalloproteinase-9 (MMP-9). Macrophage activation, in turn, modulates the fibrotic response, in part by stimulating fibroblast extracellular matrix (ECM) synthesis. We hypothesized that overexpression of human MMP-9 in mouse macrophages would amplify the inflammatory and fibrotic responses to exacerbate left ventricular dysfunction. Unexpectedly, at day 5 post-MI, ejection fraction was improved in transgenic (TG) mice (25±2%) compared to the wild type (WT) mice (18±2%; p<0.05). By gene expression profiling, 23 of 84 inflammatory genes were decreased in the left ventricle infarct (LVI) region from the TG compared to WT mice (all p<0.05). Concomitantly, TG macrophages isolated from the LVI, as well as TG peritoneal macrophages stimulated with LPS, showed decreased inflammatory marker expression compared to WT macrophages. In agreement with attenuated inflammation, only 7 of 84 cell adhesion and ECM genes were increased in the TG LVI compared to WT LVI, while 43 genes were decreased (all p<0.05). These results reveal a novel role for macrophage-derived MMP-9 in blunting the inflammatory response and limiting ECM synthesis to improve left ventricular function post-MI.
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