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199406, Ñàíêò-Ïåòåðáóðã, óë.Ãàâàíñêàÿ, ä. 49, êîðï.2

ISSN 1999-6314

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«
Vol. 12, Art. 102 (pp. 1248-1265)    |    2011       
»

Molecular mechanisms of endothelial dysfunction in venous thromboembolism: the present state and perspectives of investigation
Polyakova A. P., Blinov M. N., Kargin V. D., Kapustin S. I.

Russian Research Institute of Hematology and Transfusiology



Brief summary

Venous thromboembolism (VT) composes one of the most common groups of socially meaningful diseases in industrialized countries and is known as a multifactorial disease. Along with the classical risk factors, there are several genetic determinants of increased tendency to develop VT, which presence is described by the term “inherited thrombophilia”. The frequency of these pathological variants in patients with VT does not exceed 50%. Moreover, about one third of all VT cases appear without any known risk factor. Therefore, further studies on molecular mechanisms of VT are needed. The damage of the vessel wall, mainly endothelium lay, is described as an endothelial dysfunction and postulated to be an important step in the initiation of thrombosis. Different pathological processes could influence the integrity and functional activity of endothelium. The most probable mechanisms underlying endothelial cells injury or/and functional impairment in VT is an oxidative stress and hyperhomocysteinemia, a disturbance of a balance between vasoconstriction and vasodilatation processes, a development of proinflammatory immune response. In this study, we discuss the molecular genetic aspects of the above mentioned mechanisms which can participate in the development of endothelial dysfunction and, thus, increase the risk of VT.


Key words

venous thromboembolism, endothelium, dysfunction, gene, polymorphism





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