Damage to the Vascular Endothelium as a Leading Mechanism of COVID-19 Systemic Pathology

An analysis of the molecular and pathophysiological mechanisms of COVID-19 is presented. The endothelium of blood vessels, a kind of “endocrine tree” of the lungs and other organs in which important pathophysiological processes are concentrated, is considered as the target of the aggressive effects of the SARS-CoV-2 coronavirus. Since the main cellular target of viral aggression is the ACE2 enzyme, consideration of its role is the main line of discussion. Coronavirus blocks the activity of ACE2, a natural producer of angiotensins peptides, thus disrupting the balance of hemovascular control. Under normal conditions this mission is performed by the ACE/ACE2 complex, enzymes that control the synthesis and physiological activity of angiotensins and bradykinin peptides. Changes in the ACE/ACE2 axis ratios and cytokine stress are associated with endothelial dysfunction and a number of vascular disorders. The STORM-2 concept is proposed for the first time. According to the concept, the cause of severe organ pathology is the violation of hemostasis, transcellular diffusion, and maintenance of blood pressure.