Current knowledge regarding mechanisms underlying cardiovascular complications in patients with COVID-19 is limited and urgently needed. We shed light on a previously unrecognized mechanism and unravel a key role of red blood cells, driving vascular dysfunction in patients with COVID-19 infection. We establish the presence of profound and persistent endothelial dysfunction in vivo in patients with COVID-19. Mechanistically, we show that targeting reactive oxygen species or arginase 1 improves vascular dysfunction mediated by red blood cells. These translational observations hold promise that restoring the redox balance in red blood cells might alleviate the clinical complications of COVID-19-associated vascular dysfunction.
Keywords: ACh, acetylcholine; C19-RBC, red blood cell from patients with COVID-19; COVID-19; EDR, endothelium-dependent relaxation; EIR, endothelium-independent relaxation; H-RBC, red blood cell from healthy subjects; HNE, hydroxynonenal; IFN, interferon; RBC, red blood cell; RHI, reactive hyperemia index; ROS, reactive oxygen species; SNP, sodium nitroprusside; TNF, tumor necrosis factor; arginase; endothelial dysfunction; nitric oxide; reactive oxygen species; red blood cells.
© 2022 The Authors.