[Endothelium and vascular protection: an update]

Endothelial cells (EC) are highly specialized cells cable of modulating their functional stage in response to different stimuli. The endothelium has various atheroprotective functions: it regulates coagulation, thrombosis and the fibrinolytic system; it modulates the activity of smooth muscle cells (vascular tone/proliferation) and controls the traffic of macromolecules and inflammatory cells to the vessel wall. Impairment of these functions (endothelial dysfunction) potentiates the development of atherosclerotic lesions. High levels of plasma lipids, particularly, low-density (LDL) and very-low-density lipoproteins (VLDL) are among the pathophysiologic stimuli that induce endothelial dysfunction. LDLs have been implicated in the induction of changes in permeability, cell adhesion and secretion of vasoactive molecules (nitric oxide [NO], prostacycline [PGI2]), while VLDLs seem to modulate the fibrinolytic system [tissue plasminogen activator (t-PA) and its inhibitor (PAI-I)]. Endothelial function is controlled by a small number of genes (transcription factors) that modulate EC response to inflammatory stimuli (nuclear factor kappa beta, NF-kappabeta) or flow conditions (genes-regulated by shear-stress-responsive elements, SSREs). In addition, the control of key cellular biosynthetic pathways, such as endothelial cholesterol biosynthesis, are regulated by sterol-regulatory-elements binding proteins (SREBPs) that could be involved in the maintenance of normal endothelial function.