Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes

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 metalloprot...

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Bibliographic Details
Published in:Thrombosis and haemostasis Vol. 101; no. 6; p. 1006
Main Authors: Newby, Andrew C, George, Sarah J, Ismail, Yasmin, Johnson, Jason L, Sala-Newby, Graciela B, Thomas, Anita C
Format: Journal Article
Language:English
Published: Germany 01.06.2009
Subjects:
Animals
Aortic Rupture - etiology
Aortic Rupture - prevention & control
Atherosclerosis - complications
Atherosclerosis - enzymology
Atherosclerosis - immunology
Atherosclerosis - pathology
Foam Cells - enzymology
Foam Cells - pathology
Gene Expression Regulation, Enzymologic
Humans
Lipid Metabolism
Matrix Metalloproteinases - genetics
Matrix Metalloproteinases - metabolism
Mice
Models, Immunological
Myocardial Infarction - complications
Myocardial Infarction - enzymology
Myocardial Infarction - immunology
Myocardial Infarction - pathology
Myocytes, Smooth Muscle - pathology
Tissue Inhibitor of Metalloproteinases - immunology
Tissue Inhibitor of Metalloproteinases - metabolism
ISSN:0340-6245
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Summary: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.
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ISSN:0340-6245
DOI:10.1160/th08-07-0469