Andy
Retired committee member
Highlights
• Patients hospitalized for COVID-19 display marked impairment in endothelial function, which is persistent following recovery from the acute infection.
• Red blood cells (RBCs) from patients with COVID-19 impair vascular function through mechanisms involving increased arginase 1, reactive oxygen species (ROS) and interferon γ (IFNγ), and reduced nitric oxide (NO) bioactivity.
• These data advance our understanding in COVID-19–associated vascular injury with a clear involvement of RBCs.
• Targeting these mechanisms might provide a novel therapeutic strategy to alleviate vascular injury in patients with COVID-19.
Summary
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.
Open access, https://www.sciencedirect.com/science/article/pii/S2452302X2100396X
• Patients hospitalized for COVID-19 display marked impairment in endothelial function, which is persistent following recovery from the acute infection.
• Red blood cells (RBCs) from patients with COVID-19 impair vascular function through mechanisms involving increased arginase 1, reactive oxygen species (ROS) and interferon γ (IFNγ), and reduced nitric oxide (NO) bioactivity.
• These data advance our understanding in COVID-19–associated vascular injury with a clear involvement of RBCs.
• Targeting these mechanisms might provide a novel therapeutic strategy to alleviate vascular injury in patients with COVID-19.
Summary
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.
Open access, https://www.sciencedirect.com/science/article/pii/S2452302X2100396X