Endotheliopathy and systemic inflammation: reversibility of cause-and-effect relationship in the pathological functional system (review of literature)

Abstract

   The review considers the involvement of the endothelium and endothelial glycocalyx in the systemic inflammatory response. The role of the endothelium in the inflammation is ambivalent and depends on the nature of the inflammatory process. The physiological response of endothelial cells to local inflammation is necessary to successful eliminate the pathogen and restore the tissue homeostasis. In systemic inflammation, the endothelium is the most «suffering» structure of the body. However, endothelial cells can be a source of systemic inflammatory mediators, supporting the pathological inflammatory process. The problem of generalization of inflammation is discussed where endotheliopathy develops and closes the vicious circle, being both a consequence of systemic inflammation and the cause of its prolongation and intensification. In the pathogenesis of a new coronavirus infection the relationship between endotheliopathy and systemic inflammation was most clearly manifested. Preceding endothelial dysfunction causes a severe course of COVID-19 with a «cytokine storm» and coagulopathy that can lead to the death. SARS-CoV-2 infection induces long-term endothelial dysfunction, which is recorded even after the virus elimination. The early detection of blood level of endothelial glycocalyx damage markers (i. e. syndecan-1, glycosaminoglycans like heparan sulfate and hyaluronic acid) may seem to be an effective approach to the prevention of severe forms of COVID-19. Endothelial-protective drugs can reduce the risk of severe new coronavirus infection and eliminate the manifestations of long-COVID.