Oxidative stress-induced endothelial dysfunction and decreased vascular nitric oxide in COVID-19 patients

著者: Virginie Montiel, Irina Lobysheva, Ludovic Gérard, Marjorie Vermeersch, David Pérez‐Morga, Thomas Castelein, Jean-Baptiste Mesland, Philippe Hantson, Christine Collienne, Damien Gruson, Marie‐Astrid van Dievoet, Alexandre Persu, Christophe Beauloye, Mélanie Dechamps, Leïla Belkhir, Annie Robert, Marc Derive, Pierre‐François Laterre, A.H. Jan Danser, Xavier Wittebole, Jean‐Luc Balligand - EBioMedicine 2022 被引用: 99

BACKGROUND: SARS-CoV-2 targets endothelial cells through the angiotensin-converting enzyme 2 receptor. The resulting endothelial injury induces widespread thrombosis and microangiopathy. Nevertheless, early specific markers of endothelial dysfunction and vascular redox status in COVID-19 patients are currently missing. METHODS: Observational study including ICU and non-ICU adult COVID-19 patients admitted in hospital for acute respiratory failure, compared with control subjects matched for cardiovascular risk factors similar to ICU COVID-19 patients, and ICU septic shock patients unrelated to COVID-19. FINDINGS: = 0.13; P < 0.05). Plasma levels of angiotensin II, aldosterone, renin or serum level of TREM-1 ruled out any hyper-activation of the renin-angiotensin-aldosterone system or leucocyte respiratory burst in ICU COVID-19 patients, contrary to septic patients. INTERPRETATION: Endothelial oxidative stress with ensuing decreased NO bioavailability appears as a likely pathogenic factor of endothelial dysfunction in ICU COVID-19 patients. A correlation between NO bioavailability and oxygenation parameters is observed in hospitalized COVID-19 patients. These results highlight an urgent need for oriented research leading to a better understanding of the specific endothelial oxidative stress that occurs during SARS-CoV-2. FUNDING: Stated in the acknowledgments section.