Abstract
Plaque rupture underlies most myocardial infarctions. Plaques vulnerable to rupture have thin fibrous caps, an excess of macrophages over vascular smooth muscle cells, large lipid cores, and depletion of collagen and other matrix proteins form the cap and lipid core. Production of matrix metalloproteinases from macrophages is prominent in human plaques, and studies in genetically modified mice imply a causative role for metalloproteinases in plaque vulnerability. Recent in-vitro studies on human monocyte-derived macrophages and on foam-cell macrophages generated in vivo suggest the existence of several macrophage phenotypes with distinct patterns of metalloproteinase expression. These phenotypes could play differing roles in cap, core and aneurysm formation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aortic Rupture / etiology
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Aortic Rupture / prevention & control
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Atherosclerosis / complications
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Atherosclerosis / enzymology*
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Atherosclerosis / immunology
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Atherosclerosis / pathology*
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Foam Cells / enzymology*
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Foam Cells / pathology
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Gene Expression Regulation, Enzymologic
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Humans
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Lipid Metabolism
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Matrix Metalloproteinases / genetics
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Matrix Metalloproteinases / metabolism*
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Mice
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Models, Immunological
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Myocardial Infarction / complications
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Myocardial Infarction / enzymology
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Myocardial Infarction / immunology
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Myocardial Infarction / pathology
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Myocytes, Smooth Muscle / pathology
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Tissue Inhibitor of Metalloproteinases / immunology
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Tissue Inhibitor of Metalloproteinases / metabolism
Substances
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Tissue Inhibitor of Metalloproteinases
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Matrix Metalloproteinases