SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2

Includes images of “[r]epresentative images of vascular endothelial control cells (left) and cells treated with the SARS-CoV-2 Spike protein (right) [which] show that the spike protein causes increased mitochondrial fragmentation in vascular cells.” BBB “SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection relies on the binding of S protein (Spike glycoprotein) to ACE (angiotensin-converting enzyme) 2 in the host cells. Vascular endothelium can be infected by SARS-CoV-2, which triggers mitochondrial reactive oxygen species production and glycolytic shift. Paradoxically, ACE2 is protective in the cardiovascular system, and SARS-CoV-1 S protein promotes lung injury by decreasing the level of ACE2 in the infected lungs. In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.”