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DOI: 10.1160/TH08-07-0469
Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes
Financial support: The authors’ work is supported by the British Heart Foundation and the European Vascular Genomics Network.Publication History
Received:
23 July 2008
Accepted after minor revision:
15 January 2008
Publication Date:
24 November 2017 (online)


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 metallopro teinases 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.