Vulnerable atherosclerotic plaque metalloproteinases and foam cell phenotypes

Andrew C. Newby; Sarah J. George; Yasmin Ismail; Jason L. Johnson; Graciela B. Sala-Newby; Anita C. Thomas

doi:10.1160/TH08-07-0469

Thrombosis and Haemostasis, Table of Contents

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

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

,

Sarah J. George

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

,

Yasmin Ismail

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

,

Jason L. Johnson

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

,

Graciela B. Sala-Newby

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

,

Anita C. Thomas

¹University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK

› Author Affiliations

Abstract

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

Full Text

References

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