Abstract
Located at the interface between the vessel wall and circulating blood, the vascular endothelium plays a critical role in the homeostatic and physiologic functions of the vasculature. In response to biochemical and mechanical stimuli, endothelial cells synthesize and elaborate a number of factors that modulate vascular tone, inflammation, thrombosis, and vascular growth. Normal endothelium provides a fluid antiatherogenic environment that inhibits platelet and leukocyte adhesion, prevents vasospasm, promotes fibrinolysis, and inhibits vascular smooth muscle cell growth. Under pathologic conditions when homeostatic mechanisms are altered, the phenotypic changes that occur in endothelial cells support a vasospastic, prothrombotic, and proinflammatory milieu, and play a central role in the pathophysiology and clinical manifestation of cardiovascular disease [1].
“...the fluidity of blood within the living body depends upon the action of the walls of the vessel upon it...” (Ernst Von Brücke, 19th Century Viennese physiologist)
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Gokce, N., Loscalzo, J. (2000). Endothelial Dysfunction and Atherothrombosis. In: Wilson, P.W.F. (eds) Atlas of Atherosclerosis. Current Medicine Group, London. https://doi.org/10.1007/978-1-4757-9310-9_2
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DOI: https://doi.org/10.1007/978-1-4757-9310-9_2
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