Endothelial activation. Sliding door to atherosclerosis

The vascular endothelium has been long viewed as a simply physical separation between blood and tissue [1]. Over the last two decades a consistent bulk of data demonstrated that endothelium is a widely distributed organ, with a variable degree of heterogeneity among and within tissues [2, 3] and deeply involved in vascular physiology and pathophysiology, rather than a cellophane-like membrane that lines the circulatory system [1]. Being positioned at the interface of blood and tissue, the vascular endothelium is able to sense changes in hemodynamic forces and biochemical stimuli and promptly responds to local changes in biological needs by modulating vasomotion, hemostasis, angiogenesis, and vascular growth [1]. The vascular endothelium also modulates the trafficking of circulating blood cells by up-regulating adhesion molecules on cell surface [1, 4, 5]. These cell membrane-associated molecules are critic for leukocyte migration into specific organs under physiologic conditions and accelerate migration towards sites of inflammation [ 1, 4, 5]. Recently, the multi-step cascade of events that results in the local recruitment of leukocytes to sites of inflammatory challenge, also known as endothelial activation, has been considered as a crucial step in the initiation of atherosclerosis process, as well as in the development of advanced atherosclerosis [6].