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