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Review
. 2017 Mar 16;129(11):1415-1419.
doi: 10.1182/blood-2016-07-692673. Epub 2017 Feb 7.

Platelets and von Willebrand factor in atherogenesis

Melinda D Wu  1   2 , Tamara M Atkinson  1   3 , Jonathan R Lindner  1   4
Affiliations
Review

Platelets and von Willebrand factor in atherogenesis

Melinda D Wu et al. Blood. .

Abstract

The role of platelet adhesion, activation, and aggregation in acute atherothrombotic events such as myocardial infarction and stroke is well established. There is increasing evidence that platelet-endothelial interactions also contribute to early atherosclerotic plaque initiation and growth. Through these interactions, platelet-derived factors can contribute to the proinflammatory and mitogenic status of resident mural cells. Among the many putative mechanisms for platelet-endothelial interactions, increased endothelial-associated von Willebrand factor, particularly in a multimerized form, which interacts with platelet glycoproteins and integrins, is a major factor and represents a therapeutic target in early atherogenesis.

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Figures

Figure 1.
Figure 1.
Schematic illustration of potential mechanisms and proatherogenic effects of platelet-endothelial interactions. EC, endothelial cell; LDL, low-density lipoprotein; UL, ultralarge.
See this image and copyright information in PMC

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References

    1. Gryglewski RJ, Chłopicki S, Uracz W, Marcinkiewicz E. Significance of endothelial prostacyclin and nitric oxide in peripheral and pulmonary circulation. Med Sci Monit. 2001;7(1):1-16. - PubMed
    1. Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation. 2004;109(23 suppl 1):III27-III32. - PubMed
    1. Kanthi Y, Hyman MC, Liao H, et al. . Flow-dependent expression of ectonucleotide tri(di)phosphohydrolase-1 and suppression of atherosclerosis. J Clin Invest. 2015;125(8):3027-3036. - PMC - PubMed
    1. Borissoff JI, Spronk HM, ten Cate H. The hemostatic system as a modulator of atherosclerosis. N Engl J Med. 2011;364(18):1746-1760. - PubMed
    1. Laszik ZG, Zhou XJ, Ferrell GL, Silva FG, Esmon CT. Down-regulation of endothelial expression of endothelial cell protein C receptor and thrombomodulin in coronary atherosclerosis. Am J Pathol. 2001;159(3):797-802. - PMC - PubMed

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