Figure 3.

SARS-CoV-2 infection causes inflammation of vascular endothelial cells. After SARS-CoV-2 enters endothelial cells from ACE2, it promotes the reduction of ACE2 on the cell surface, which in turn leads to an increase in AngII in the blood, a decrease in local anti-inflammatory ability, and an increase in the expression of cytokines such as TNF-α, IL-6, and IL-1. Overexpression of inflammatory factors leads to the damage of vascular endothelial cells and the formation of a local procoagulant state. On the other hand, SARS-CoV-2 causes ACE1 to fall off the cell surface at the initial stage of infection, which promotes local plasma leakage and the expression of inflammatory factors. As the free ACE1 drops to a very low level, ACE2 is induced, which, in turn, promotes SARS-CoV-2 to enter endothelial cells. A vicious cycle between SARS-CoV-2 infection and overexpression of inflammatory factors forms.