Review Article Role of Matrix Metalloproteinase-8 in Atherosclerosis

Copyright © 2013 Sébastien Lenglet et al. is 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 in�amed, and collagen-poor �brous caps and contain elevated levels of proteases, including metalloproteinases (MMPs). Initiation of collagen breakdown in plaques requires interstitial collagenases, aMMP subfamily consisting ofMMP-1,MMP-8, andMMP-13. Previous reports demonstrated thatMMP-1 andMMP-13might be overexpressed in both human and experimental atherosclerosis. Since neutrophils have been only recently reported in atherosclerotic plaques, the role ofMMP-8 (formerly known as “neutrophil collagenase”) was onlymarginally evaluated. In this paper, we will update and comment on evidence of themost relevant regulatory pathways and activities mediated byMMP-8 in atherogenesis. 1