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Exp Clin Cardiol. 2011 Fall;16(3):77-86.

An integrated approach for the mechanisms responsible for atherosclerotic plaque regression.

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  • 1Institute of Cardiovascular Sciences, St Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba.


Atherosclerosis was originally considered to be an ongoing process that was inevitably associated with age. However, plaques are highly dynamic, and are able to progress, stabilize or regress depending on their surrounding milieu. A great deal of research attention has been focused on understanding the involvement of high-density lipoprotein in atherosclerotic plaque regression. However, atherosclerotic plaque regression encompasses a variety of processes that can be grouped into three main areas: removal of lipids and necrotic material; restoration of endothelial function and repair of denuded areas; and cessation of vascular smooth muscle cell proliferation and phenotype reversal. In addition to the role of high-density lipoproteins in lipid removal, resident macrophages and foam cells are able to regain motility and rapidly migrate on milieu improvement, moving both lipids and necrotic material to regional lymph nodes. Neighbouring endothelial cells can proliferate and replace dead and dysfunctional cells. Circulating endothelial progenitor cells can similarly restore vessel function. Finally, abrogation of smooth muscle cell proliferation occurs secondarily to these processes. This information is integrated in the current article to present a comprehensive and clear depiction of plaque regression. This integrated view of regression is essential to optimize the pharmaceutical targeting of the many processes and pathways involved in plaque regression.


Atherosclerosis; Endothelium; Macrophage migration; Regression; Reverse cholesterol transport; Smooth muscle cells

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