ArticleCirculation2011
Reduced degradation of the chemokine MCP-3 by matrix metalloproteinase-2 exacerbates myocardial inflammation in experimental viral cardiomyopathy.
Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Genetically predicted associations between inflammatory cytokines and juvenile idiopathic arthritis: A Mendelian randomization study.Medicine · 2026Pooled it
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Monocytes and interstitial macrophages contribute to hypoxic pulmonary hypertension.The Journal of clinical investigation · 2025Article
- Coronavirus disease 2019-related myocardial injury is associated with immune dysregulation in symptomatic patients with cardiac magnetic resonance imaging abnormalities.Cardiovascular research · 2024Observational
- Association of plasma proteomics with mortality in individuals with and without type 2 diabetes: Results from two population-based KORA cohort studies.BMC medicine · 2024Article
- Low-dose pro-resolving mediators temporally reset the resolution response to microbial inflammation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Self-recruited neutrophils trigger over-activated innate immune response and phenotypic change of cardiomyocytes in fulminant viral myocarditis.Cell discovery · 2023Article
- Hesperetin attenuates LPS-induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway.Immunity, inflammation and disease · 2023Article
- Matrix metalloproteinases in coronary artery disease and myocardial infarction.Basic research in cardiology · 2023Review
- Pathophysiological Mechanisms of Cardiac Dysfunction in Transgenic Mice with Viral Myocarditis.Cells · 2023Article
- Multidisciplinary diagnostic approach for fulminant myocarditis related to coronavirus disease 2019 messenger RNA vaccines: a case report.European heart journal. Case reports · 2023Article
- AAV9-mediated functional screening for cardioprotective cytokines in Coxsackievirus-B3-induced myocarditis.Scientific reports · 2022Article
- Left ventricle- and skeletal muscle-derived fibroblasts exhibit a differential inflammatory and metabolic responsiveness to interleukin-6.Frontiers in immunology · 2022Article
- Viral Myocarditis-From Pathophysiology to Treatment.Journal of clinical medicine · 2021Review
- CCL7 contributes to angiotensin II-induced abdominal aortic aneurysm by promoting macrophage infiltration and pro-inflammatory phenotype.Journal of cellular and molecular medicine · 2021Article
- Article
- Review
- The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.Cardiovascular diagnosis and therapy · 2020Article
- Modulation of the acute defence reaction by eplerenone prevents cardiac disease progression in viral myocarditis.ESC heart failure · 2020Article
- Precursor proadrenomedullin influences cardiomyocyte survival and local inflammation related to myocardial infarction.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocarditis is an important cause for cardiac failure, especially in younger patients, followed by the development of cardiac dysfunction and death. The present study investigated whether gene deletion of matrix metalloproteinase-2 influences cardiac inflammation and function in murine coxsackievirus B3 (CVB3)-induced myocarditis. METHODS AND
resultsMatrix metalloproteinase-2 knockout mice (MMP-2(-/-)) and their wild-type controls (WT) were infected with CVB3 to induce myocarditis. Three days after infection, an increased invasion of CD4(+)-activated T cells into the myocardium was documented, followed by an excess of inflammatory cells 7 days after infection, which was significantly higher in the MMP-2(-/-)animals compared with the WT animals. Moreover, cardiac apoptosis, remodeling, viral load, and function were deteriorated in MMP-2(-/-) animals after CVB3 infection. This overwhelming inflammation was followed by 100% mortality after 15 days. This was associated with increased levels of MCP-3 in the cardiac tissue of MMP-2(-/-) mice. Because MMP-2 cleaves the chemokine MCP-3, the loss of this cleavage lead to an overreaction of the immune system with pronounced myocardial damage mediated by the inflammatory cells. When a neutralizing antibody against MCP-3 was given to MMP-2(-/-) mice, this exaggerated reaction of the immune system could be normalized to levels similar to WT-CVB3 animals.
conclusionsLoss of MMP-2 increased the inflammatory response after CVB3 infection, which impaired cardiac function and survival during CVB3-induced myocarditis. Matrix metalloproteinase-2-mediated chemokine cleavage has an important role in cardiac inflammation as a negative feedback mechanism.
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