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

Authors: Yuyang LeiJiao ZhangCara R. SchiavonMing HeLili ChenHui ShenYichi ZhangQian YinYoshitake ChoLeonardo AndradeGerald S. ShadelMark HepokoskiTing LeiHongliang WangJin ZhangJason X., et. al.

SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection relies on the binding of S protein (Sprotein (Spike glycoprotein) to ACE (angiotensin-converting enzyme) 2 in the host cells. Vascular endothelium can be infected by SARS-CoV-2,1 which triggers mitochondrial reactive oxygen species production and glycolytic shift.2 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.3 In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

For More Information: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.121.318902

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