Abstract
See related article, pages 149–156 In this issue of Circulation Research , Woollard et al identify a critical role of pathologically elevated levels of soluble P-selectin (sP-selectin) found in the plasma of patients with peripheral arterial occlusive disease (PAOD) that promotes the activation of neutrophils and induces their adhesion to fibrinogen and platelet monolayers.1 P-selectin is an inflammatory adhesion molecule expressed on activated platelets and endothelial cells.2 During the last two decades, the role of inflammatory cells and adhesion molecules in the development and progression of vascular diseases has become apparent, and it is now recognized that many of the cellular and molecular events that underlie atherosclerotic vascular disease are inflammatory in nature.3,4 One manifestation of atherosclerosis is PAOD, which is characterized by intermittent claudication and critical limb ischemia.5 The first case of intermittent claudication caused by arterial occlusive disease was described as early as 1831 by Jean Bouley, and a few years later Heinrich Erb proposed walking as a therapy for intermittent claudication6; however, the precise mechanism of development of PAOD as well as the optimal treatments of this disease still remain to be determined. Numerous studies have identified soluble inflammatory markers including acute phase proteins and adhesion molecules as risk factors for cardiovascular disease, but it is unclear whether they play causative roles as active participants in the initiation and maintenance of the inflammation (mediators) or whether they merely indicate the existence of the disease (markers). Soluble P-selectin is elevated in patients with vascular disorders such as hypertension,7 hypercholesterolaemia, …
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