Endothelial dysfunction in COVID-19 (literature review)

It has been repeatedly confirmed that the virus SARS-CoV-2 — the cause of a pandemic COVID-19 worldwide — is involved in the development or aggravation of existing endothelial dysfunction. The main route of penetration of the virus into the human body are ACE2 receptors, which are expressed, including on endothelial cells. Once in the host cells, SARS-CoV-2 stimulates the processes of local inflammation, as a result of which cytokines begin to be intensively released, which in turn also have a negative effect on the endothelium. The cytokine storm-activated complement pathways lead to even greater synthesis of cytokines, as well as increased production of adhesion molecules. The inflammatory process in endothelial cells stimulates procoagulant, prothrombotic and antifibrinolytic factors that adversely affect the blood coagulation process. In addition, excessive synthesis of vasoconstrictor factors by activated endothelium promotes hypercoagulated processes in the body. The article discusses the main mechanisms for the development of endothelial dysfunction in COVID-19. Understanding the pathogenesis of this pathology will make it possible to identify certain aspects of treatment and prevention of complications in patients with COVID-19, which will help to cope with complications and high mortality from this disease.

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