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<ns3:p>Activation, dysfunction and damage to the vascular endothelium play a key role in pathogenesis ofcardiovasculatory diseases and inflammatory diseases of the blood vessels. Disturbances in the functioningand structure of the endothelium also occur in hypertension, infectious diseases, cancers and some bleedingdisorders. Endothelial activation is expressed with an increase of its permeability to water, lipoproteins andplasma proteins as well as an increased expression of adhesion molecules on the surface of endothelial cells.Expression of adhesion molecules on the endothelium allows the leukocytes to adhere and migrate into thevascular wall initiating inflammation. Adhesion molecules: E-selectin, P-selectin, vascular cell adhesion molecule(VCAM), intercellular adhesion molecule (ICAM) are considered to be laboratory markers of endothelial activation.Endothelial dysfunction is characterized by the disappearance of its functional integrity. It is expressed by animbalance between the production of vasodilating and vasoconstricting compounds in the endothelium as wellas an imbalance between the production of antithrombotic and prothrombotic compounds. Laboratory markersof endothelial dysfunction are reduced nitric oxide concentration or increased endothelin-1 concentration.Cellular damage is the most advanced degree of endothelial dysfunction. It is characterized by structuralchanges or detachment of endothelial cells from the basal lamina. Biochemical markers of endothelial damagethat are analyzed the most are haemostatic factors released from the damaged cells: von Willebrand factor andthrombomodulin, while the morphological marker of its damage are circulating endothelial cells. The aim of thestudy was to review data on the structure, function and methods of determining biomarkers that can be used inthe assessment of endothelial dysfunction and damage.</ns3:p>