ArticleArteriosclerosis, thrombosis, and vascular biology2013
Impaired coronary collateral growth in the metabolic syndrome is in part mediated by matrix metalloproteinase 12-dependent production of endostatin and angiostatin.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond.Journal of molecular and cellular cardiology · 2024Review
- Increased Plasma Non-High-Density Lipoprotein Levels and Poor Coronary Collateral Circulation in Patients With Stable Coronary Artery Disease.Texas Heart Institute journal · 2023Article
- Metabolic syndrome and its components reduce coronary collateralization in chronic total occlusion: An observational study.Cardiovascular diabetology · 2021Observational
- Simultaneous Upregulation of Elastolytic and Elastogenic Factors Are Necessary for Regulated Collateral Diameter Expansion.Frontiers in cardiovascular medicine · 2021Article
- Superimposition of metabolic syndrome magnifies post-stenotic kidney injury in dyslipidemic pigs.American journal of translational research · 2021Article
- Cardioprotection during ischemia by coronary collateral growth.American journal of physiology. Heart and circulatory physiology · 2019Review
- Elevated 20-HETE in metabolic syndrome regulates arterial stiffness and systolic hypertension via MMP12 activation.Journal of molecular and cellular cardiology · 2018Article
- Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2017Article
- Associations between circulating endostatin levels and vascular organ damage in systemic sclerosis and mixed connective tissue disease: an observational study.Arthritis research & therapy · 2015Observational
- miR-21-mediated decreased neutrophil apoptosis is a determinant of impaired coronary collateral growth in metabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2015Article
- Regulation of signal transduction by reactive oxygen species in the cardiovascular system.Circulation research · 2015Review
- miR-21 normalizes vascular smooth muscle proliferation and improves coronary collateral growth in metabolic syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe have previously shown that transient coronary artery occlusion stimulated coronary collateral growth (CCG) in healthy (Sprague Dawley) but not in metabolic syndrome (JCR:LA-cp [JCR] ) rats. Here, we sought to determine whether matrix metalloproteinases (MMPs) negatively regulate CCG in the metabolic syndrome via release of endostatin and angiostatin. APPROACH AND
resultsRats underwent transient, repetitive left anterior descending occlusion and resultant myocardial ischemia (RI) for 0 to 10 days. CCG was measured in the collateral-dependent and normal zones using microspheres, MMP activation by Western blot, and endostatin and angiostatin by ELISA on days 0, 3, 6, 9, or 10 of RI. Endostatin and angiostatin were increased in JCR but not in Sprague Dawley rats on days 6 and 9 of RI. Increased endostatin and angiostatin correlated with increased MMP12 (≈ 4-fold) activation in JCR but not in Sprague Dawley rats on days 6 and 9 of RI. Inhibition of MMP12 in JCR rats nearly completely blocked endostatin (≈ 85%) and angiostatin (≈ 90%) generation and significantly improved CCG (collateral-dependent zone flow was ≈ 66% of normal zone flow versus ≈ 12% for JCR RI).
conclusionsCompromised CCG in the metabolic syndrome is, in large part, because of increased MMP12 activation and consequent increased generation of endostatin and angiostatin, which inhibits late-stage collateral remodeling.
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