期刊
EUROPEAN HEART JOURNAL
卷 24, 期 24, 页码 2166-2179出版社
OXFORD UNIV PRESS
DOI: 10.1016/j.ehj.2003.08.021
关键词
P-setectin; atherosclerosis; platelet activation
The adhesion molecule P-setectin (CD62P) is of interest because of its role in modulating interactions between blood cells and the endothelium, and also because of the possible use of the soluble form as a plasma predictor of adverse cardiovascutar events. Although present on the external cell surface of both activated endothetium and activated platelets, it now seems clear that most, if not all, of the measured plasma P-selectin is of platelet origin. P-selectin is partially responsible for the adhesion of certain leukocytes and platelets to the endothelium. Animal models have also shown the important rote of P-setectin in the process of atherogenesis. For example, increased P-setectin expression has been demonstrated on active atherosclerotic plaques; in contrast, fibrotic inactive plaques tack P-setectin expression, and animals tacking P-setectin have a decreased tendency to form atherosclerotic plaques. Increased levels of soluble P-setectin in the plasma have also been demonstrated in a variety of cardiovascular disorders, including coronary artery disease, hypertension and atrial fibrillation, with some relationship to prognosis. The objective of this review is to provide an overview of the current literature on this molecule and thus present a concise view of its potential in dissecting the pathophysiology of atherosclerosis. In doing so we shalt focus primarity on human biology but will note a small number of excellent lessons provided by non-human work. (C) 2003 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
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