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Thromb Haemost 2009; 101(06): 1006-1011
DOI: 10.1160/TH08-07-0469
Theme Issue Article
Schattauer GmbH

Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes

Andrew C. Newby
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
,
Sarah J. George
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
,
Yasmin Ismail
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
,
Jason L. Johnson
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
,
Graciela B. Sala-Newby
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
,
Anita C. Thomas
1   University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
› Author AffiliationsFinancial support: The authors’ work is supported by the British Heart Foundation and the European Vascular Genomics Network.
Further Information

Publication History

Received: 23 July 2008

Accepted after minor revision: 15 January 2008

Publication Date:
24 November 2017 (online)

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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 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.

Keywords

Atherosclerosis - atherothrombosis - extracellular matrix - inflammation - matrix metalloproteinases
 

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