ArticlePloS one2017
Metalloproteinase-9 contributes to endothelial dysfunction in atherosclerosis via protease activated receptor-1.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Smoking and Unstable Plaque in Acute Coronary Syndrome: A Systematic Review of The Role of Matrix Metalloproteinases.International journal of medical sciences · 2023Pooled it
- Citrus Peel Xanthophylls Orchestrate Lipid-Glucose-Inflammation Axis Reprogramming in Cardiometabolic Syndrome: Integrative In Silico and In Vivo Evidence.Molecular nutrition & food research · 2026Article
- Defining the Systemic Response to Flight After Polytrauma in a Murine Model.Military medicine · 2026Article
- Conjunctival Venular Hemodynamic Biomarkers in Glaucoma.Translational vision science & technology · 2025Article
- Revealing the impact ofFrontiers in immunology · 2025Article
- Effects of dengue virus type-2 serotype (DENV-2) on the expression profile of matrix metalloproteinases in THP-1, monocyte cells and their roles in endothelial dysfunctions: protective effect of atorvastatin.Frontiers in cellular and infection microbiology · 2025Article
- Human leukocyte antigen class I antibody-activated endothelium promotes CD206+ M2 macrophage polarization and MMP9 secretion through TLR4 signaling and P-selectin in a model of antibody-mediated rejection and allograft vasculopathy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Matrix metallopeptidase 9 contributes to the beginning of plaque and is a potential biomarker for the early identification of atherosclerosis in asymptomatic patients with diabetes.Frontiers in endocrinology · 2024Observational
- Mitochondrial-targeted antioxidant attenuates preeclampsia-like phenotypes induced by syncytiotrophoblast-specific Gαq signaling.Science advances · 2023Article
- Superoxide-Mediated Upregulation of MMP9 Participates in BMPR2 Destabilization and Pulmonary Hypertension Development.Antioxidants (Basel, Switzerland) · 2023Article
- ADAMTS-7 Modulates Atherosclerotic Plaque Formation by Degradation of TIMP-1.Circulation research · 2023Article
- Vascular Aging and COVID-19.Angiology · 2023Review
- Smoking Induces the Circulating Levels of Matrix Metalloproteinase-9 and Its Association with Cardiovascular Risk in Young Smokers.Medeniyet medical journal · 2022Article
- The Role of the Coagulation System in Peripheral Arterial Disease: Interactions with the Arterial Wall and Its Vascular Microenvironment and Implications for Rational Therapies.International journal of molecular sciences · 2022Review
- Discovery of four plasmatic biomarkers potentially predicting cardiovascular outcome in peripheral artery disease.Scientific reports · 2022Observational
- Theories and Molecular Basis of Vascular Aging: A Review of the Literature from VascAgeNet Group on Pathophysiological Mechanisms of Vascular Aging.International journal of molecular sciences · 2022Review
- Endothelial Foxp1 Regulates Neointimal Hyperplasia Via Matrix Metalloproteinase-9/Cyclin Dependent Kinase Inhibitor 1B Signal Pathway.Journal of the American Heart Association · 2022Article
- Article
- Thioredoxin-1 and Correlations of the Plasma Cytokines Regarding Aortic Valve Stenosis Severity.Biomedicines · 2021Article
- Interference of LPSCells · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The atherosclerotic process begins when vascular endothelial cells undergo pro-inflammatory changes such as aberrant activation to dysfunctional phenotypes and apoptosis, leading to loss of vascular integrity. Our laboratory has demonstrated that exposure of mice to second hand smoke triggers an increase in expression of metalloproteinase-9. Further, metalloproteinase-9 released by second hand smoke-activated leukocytes may propagate pro-atherogenic alterations in endothelial cells. We have shown that levels of metalloproteinase-9 were increased in the plasma from apolipoprotein E deficient (ApoE-/-) mice exposed to second hand smoke relative to non-exposed controls. Moreover, we have collected data from two different, but complementary, treatments of second hand smoke exposed atherosclerotic mice. Animals received either cell specific metalloproteinase-9 directed siRNA to minimize metalloproteinase-9 expression in neutrophils and endothelial cells, or a pharmacological inhibitor of Bruton's tyrosine kinase which indirectly limits metalloproteinase-9 production in neutrophils. These treatments reduced atherosclerotic changes in mice and improved overall vascular health. We also demonstrated that metalloproteinase-9 could activate endothelial cells and induce their apoptosis via cleavage of protease activated receptor-1. In summary, better understanding of metalloproteinase-9's pathogenic capabilities as well as novel signaling pathways involved may lead to development of treatments which may provide additional benefits to atherosclerosis patients with a history of second hand smoke exposure.
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