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Mediators of Inflammation
Volume 2013, Article ID 659282, 6 pages
Review Article

Role of Matrix Metalloproteinase-8 in Atherosclerosis

1Cardiology Division, Department of Medicine, Geneva University Hospital, Foundation for Medical Research, 1211 Geneva 4, Switzerland
2Clinic of Internal Medicine 1, Department of Internal Medicine, University of Genoa, 16100 Genoa, Italy

Received 22 September 2012; Accepted 20 December 2012

Academic Editor: Jane Stubbe

Copyright © 2013 Sébastien Lenglet et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Plaque rupture is the main cause of acute myocardial infarction and stroke. Atherosclerotic plaques have been described to be vulnerable and more prone to rupture when they are characterized by thin, highly inflamed, and collagen-poor fibrous caps and contain elevated levels of proteases, including metalloproteinases (MMPs). Initiation of collagen breakdown in plaques requires interstitial collagenases, a MMP subfamily consisting of MMP-1, MMP-8, and MMP-13. Previous reports demonstrated that MMP-1 and MMP-13 might be overexpressed in both human and experimental atherosclerosis. Since neutrophils have been only recently reported in atherosclerotic plaques, the role of MMP-8 (formerly known as “neutrophil collagenase”) was only marginally evaluated. In this paper, we will update and comment on evidence of the most relevant regulatory pathways and activities mediated by MMP-8 in atherogenesis.