International Journal of Gerontology
Volume 1, Issue 3 , Pages 103-111, September 2007

Role Of Metalloproteinases in Plaque Rupture

  • Andrew C Newby

      Affiliations

    • Corresponding Author InformationCorrespondence to: Professor Andrew Newby, Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW, UK

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

Accepted 30 June 2007.

Article Outline

SUMMARY 

Rupture of the fibrous cap over an atherosclerotic plaque is the main cause of myocardial infarctions and strokes. Plaques vulnerable to rupture have a relatively thin fibrous cap, are highly inflamed and contain less structural collagen. This suggests that increased production of proteases, including metalloproteinases (MMPs), in response to inflammation is responsible for weakening the plaque cap. If so, then MMPs or the inflammatory mediators that lead to their overexpression are attractive targets for plaque stabilizing therapy. On the other hand, remodeling of extracellular matrix and cell surface proteins promotes migration and proliferation of endothelial and smooth muscle cells which could promote vascular repair and therefore plaque stability. Greater understanding of the role of individual MMPs and the regulation of their production is therefore needed to refine therapeutic approaches.

Key Words:  atherosclerotic plaque , fibrous cap , metalloproteinases

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PII: S1873-9598(08)70030-9

doi:10.1016/S1873-9598(08)70030-9

International Journal of Gerontology
Volume 1, Issue 3 , Pages 103-111, September 2007