TY - JOUR
TI - Soluble ACE2 is upregulated and soluble eNOS is downregulated in COVID-19-induced ARDS
AU - Vassiliou, A.G.
AU - Zacharis, A.
AU - Keskinidou, C.
AU - Jahaj, E.
AU - Pratikaki, M.
AU - Gallos, P.
AU - Dimopoulou, I.
AU - Kotanidou, A.
AU - Orfanos, S.E.
JO - Pharmaceutics
PY - 2021
VL - 14
TODO - 7
SP - null
PB - MDPI AG
SN - 1999-4923
TODO - 10.3390/ph14070695
TODO - adrenomedullin;  angiotensin converting enzyme 2;  endothelial nitric oxide synthase, adult;  adult respiratory distress syndrome;  Article;  cohort analysis;  comparative study;  controlled study;  coronavirus disease 2019;  disease severity;  down regulation;  enzyme activity;  enzyme mechanism;  female;  hospital admission;  hospitalization;  human;  intensive care unit;  major clinical study;  male;  middle aged;  observational study;  pathogenesis;  protein blood level;  upregulation
TODO - A damaged endothelium is an underlying condition of the many complications of COVID-19 patients. The increased mortality risk associated with diseases that have underlying endothelial dysfunction, such as acute respiratory distress syndrome (ARDS), suggests that endothelial (e) nitric oxide synthase (NOS)-derived nitric oxide could be an important defense mechanism. Additionally, intravenous recombinant angiotensin converting enzyme 2 (ACE2) was recently reported as an effective therapy in severe COVID-19, by blocking viral entry, and thus reducing lung injury. Very few studies exist on the prognostic value of endothelium-related protective molecules in severe COVID-19 disease. To this end, serum levels of eNOS, inducible (i) NOS, adrenomedullin (ADM), soluble (s) ACE2 levels, and serum (s) ACE activity were measured on hospital admission in 89 COVID-19 patients, hospitalized either in a ward or ICU, of whom 68 had ARDS, while 21 did not. In our cohort, the COVID-19-ARDS patients had considerably lower eNOS levels compared to the COVID-19 non-ARDS patients. On the other hand, sACE2 was significantly higher in the ARDS patients. iNOS, ADM and sACE activity did not differ. Our results might support the notion of two distinct defense mechanisms in COVID-19-derived ARDS; eNOS-derived nitric oxide could be one of them, while the dramatic rise in sACE2 may also represent an endogenous mechanism involved in severe COVID-19 complications, such as ARDS. These results could provide insight to therapeutical applications in COVID-19. © 2021 by the authors.
ER -