Key result
Endogenous nitric oxide plays a dual role in COVID-19, where eNOS uncoupling causes endothelial dysfunction while increased iNOS activity offers antiviral benefits but potential pro-inflammatory harm.
Its licence doesn't allow us to show a copy here.
Why the study?
SARS-CoV-2 infection causes excessive inflammation, endothelial dysfunction, altered eNOS and iNOS activity, and downstream respiratory and vascular consequences, warranting examination of endogenous NO roles and NO-targeted therapies.
This review highlights the complex, dual role of nitric oxide in COVID-19 pathogenesis and suggests that modulating NO metabolism could be a therapeutic strategy for respiratory and vascular complications.
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.
No takes yet. Share an insight, caveat, or question.
Guimarães et al. (2021) conducted a review in COVID-19. Nitric Oxide (NO) therapies and endogenous NO metabolism was evaluated. Endogenous nitric oxide plays a dual role in COVID-19, where eNOS uncoupling causes endothelial dysfunction while increased iNOS activity offers antiviral benefits but potential pro-inflammatory harm.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: