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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Podrobná bibliografie
Vydáno v:	Thrombosis and haemostasis Ročník 101; číslo 6; s. 1006
Hlavní autoři:	Newby, Andrew C, George, Sarah J, Ismail, Yasmin, Johnson, Jason L, Sala-Newby, Graciela B, Thomas, Anita C
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Germany 01.06.2009
Témata:	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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Popis
Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0340-6245
DOI:	10.1160/th08-07-0469