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10.1016/j.niox.2021.04.003

http://scihub22266oqcxt.onion/10.1016/j.niox.2021.04.003
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33831567!8021449!33831567
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suck abstract from ncbi


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pmid33831567      Nitric+Oxide 2021 ; 111-112 (ä): 64-71
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  • Implications of SARS-Cov-2 infection on eNOS and iNOS activity: Consequences for the respiratory and vascular systems #MMPMID33831567
  • Guimaraes LMF; Rossini CVT; Lameu C
  • Nitric Oxide 2021[Jun]; 111-112 (ä): 64-71 PMID33831567show ga
  • Symptoms of COVID-19 range from asymptomatic/mild symptoms to severe illness and death, consequence of an excessive inflammatory process triggered by SARS-CoV-2 infection. The diffuse inflammation leads to endothelium dysfunction in pulmonary blood vessels, uncoupling eNOS activity, lowering NO production, causing pulmonary physiological alterations and coagulopathy. On the other hand, iNOS activity is increased, which may be advantageous for host defense, once NO plays antiviral effects. However, overproduction of NO may be deleterious, generating a pro-inflammatory effect. In this review, we discussed the role of endogenous NO as a protective or deleterious agent of the respiratory and vascular systems, the most affected in COVID-19 patients, focusing on eNOS and iNOS roles. We also reviewed the currently available NO therapies and pointed out possible alternative treatments targeting NO metabolism, which could help mitigate health crises in the present and future CoV's spillovers.
  • |*SARS-CoV-2[MESH]
  • |Blood Vessels/metabolism[MESH]
  • |COVID-19/*metabolism[MESH]
  • |Gene Expression Regulation, Enzymologic[MESH]
  • |Humans[MESH]
  • |Nitric Oxide Synthase Type II/genetics/*metabolism[MESH]
  • |Nitric Oxide Synthase Type III/genetics/*metabolism[MESH]
  • |Nitric Oxide/*metabolism[MESH]


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