ArticleMediators of inflammation2014
Relationship of MMP-14 and TIMP-3 expression with macrophage activation and human atherosclerotic plaque vulnerability.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- The Effect of Granulocyte Colony-Stimulating Factor on the Progression of Atherosclerosis in Animal Models: A Meta-Analysis.BioMed research international · 2017Pooled it
- Myeloid MMP14 couples extracellular proteolysis to inflammatory and metabolic remodeling during obesity.Cell reports · 2026Article
- Loss of IGFBP-6 promotes monocyte-driven atherogenesis in periodontal disease.Scientific reports · 2026Article
- Cholesterol-Inflammation Fusion Hypothesis in Atherosclerosis: An Evolving Paradigm in Pathogenesis and Therapy.JACC. Asia · 2026Review
- Interleukin-16 upregulates tissue inhibitor of metalloproteinase 3 to promote atherosclerotic plaque stability.Journal of translational medicine · 2026Article
- Epigenetic regulation of TIMP-3 expression in human macrophages via physiological and pharmacological modification of histone3 lysine27 (H3K27).Molecular biology reports · 2025Article
- Phenotyping atherosclerotic plaque and perivascular adipose tissue: signalling pathways and clinical biomarkers in atherosclerosis.Nature reviews. Cardiology · 2025Review
- Analysis and validation of biomarkers and immune cell infiltration profiles in unstable coronary atherosclerotic plaques using bioinformatics and machine learning.Frontiers in cardiovascular medicine · 2025Article
- MiRNA-34a, miRNA-145, and miRNA-222 Expression, Matrix Metalloproteinases, TNF-α and VEGF in Patients with Different Phenotypes of Coronary Artery Disease.International journal of molecular sciences · 2024Observational
- Role of macrophage in ocular neovascularization.Heliyon · 2024Review
- The TIMP protein family: diverse roles in pathophysiology.American journal of physiology. Cell physiology · 2024Review
- Novel Therapeutic Approaches to Prevent Atherothrombotic Ischemic Stroke in Patients with Carotid Atherosclerosis.International journal of molecular sciences · 2023Review
- Myeloid CD40 deficiency reduces atherosclerosis by impairing macrophages' transition into a pro-inflammatory state.Cardiovascular research · 2023Article
- The Nonproteolytic Intracellular Domain of Membrane-Type 1 Matrix Metalloproteinase Coordinately Modulates Abdominal Aortic Aneurysm and Atherosclerosis in Mice-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022Review
- Disparate effects of MMP and TIMP modulation on coronary atherosclerosis and associated myocardial fibrosis.Scientific reports · 2021Article
- Membrane-type I matrix metalloproteinase (MT1-MMP), lipid metabolism, and therapeutic implications.Journal of molecular cell biology · 2021Review
- Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021Review
- Different Approaches in Therapy Aiming to Stabilize an Unstable Atherosclerotic Plaque.International journal of molecular sciences · 2021Review
- Overexpressed miR-335-5p reduces atherosclerotic vulnerable plaque formation in acute coronary syndrome.Journal of clinical laboratory analysis · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Matrix metalloproteinase-14 (MMP-14) promotes vulnerable plaque morphology in mice, whereas tissue inhibitor of metalloproteinases-3 (TIMP-3) overexpression is protective. MMP-14(hi) TIMP-3(lo) rabbit foam cells are more invasive and more prone to apoptosis than MMP-14(lo) TIMP-3(hi) cells. We investigated the implications of these findings for human atherosclerosis. In vitro generated macrophages and foam-cell macrophages, together with atherosclerotic plaques characterised as unstable or stable, were examined for expression of MMP-14, TIMP-3, and inflammatory markers. Proinflammatory stimuli increased MMP-14 and decreased TIMP-3 mRNA and protein expression in human macrophages. However, conversion to foam-cells with oxidized LDL increased MMP-14 and decreased TIMP-3 protein, independently of inflammatory mediators and partly through posttranscriptional mechanisms. Within atherosclerotic plaques, MMP-14 was prominent in foam-cells with either pro- or anti-inflammatory macrophage markers, whereas TIMP-3 was present in less foamy macrophages and colocalised with CD206. MMP-14 positive macrophages were more abundant whereas TIMP-3 positive macrophages were less abundant in plaques histologically designated as rupture prone. We conclude that foam-cells characterised by high MMP-14 and low TIMP-3 expression are prevalent in rupture-prone atherosclerotic plaques, independent of pro- or anti-inflammatory activation. Therefore reducing MMP-14 activity and increasing that of TIMP-3 could be valid therapeutic approaches to reduce plaque rupture and myocardial infarction.
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