Why the study?
The contribution of the renin-angiotensin system through arachidonic acid pathway metabolites in the pathogenesis of COVID-19 was unknown.
Do plasma levels of renin-angiotensin system components and arachidonic acid metabolites differ between COVID-19 patients and healthy controls?
Do plasma levels of renin-angiotensin system components and arachidonic acid metabolites differ between COVID-19 patients and healthy controls?
COVID-19 is associated with significant dysregulation of the renin-angiotensin system and arachidonic acid pathways, suggesting these metabolites could serve as biomarkers for the disease.
Exploratory data link RAS-ArA metabolites to COVID-19; leaves open biomarker validation and clinical utility.
Through the ACE2, a main enzyme of the renin-angiotensin system (RAS), SARS-CoV-2 gains access into the cell, resulting in different complications which may extend beyond the RAS and impact the Arachidonic Acid (ArA) pathway. The contribution of the RAS through ArA pathways metabolites in the pathogenesis of COVID-19 is unknown. We investigated whether RAS components and ArA metabolites can be considered biomarkers of COVID-19. We measured the plasma levels of RAS and ArA metabolites using an LC-MS/MS. Results indicate that Ang 1-7 levels were significantly lower, whereas Ang II levels were higher in the COVID-19 patients than in healthy control individuals. The ratio of Ang 1-7/Ang II as an indicator of the RAS classical and protective arms balance was dramatically lower in COVID-19 patients. There was no significant increase in inflammatory 19-HETE and 20-HETE levels. The concentration of EETs was significantly increased in COVID-19 patients, whereas the DHETs concentration was repressed. Their plasma levels were correlated with Ang II concentration in COVID-19 patients. In conclusion, evaluating the RAS and ArA pathway biomarkers could provide helpful information for the early detection of high-risk groups, avoid delayed medical attention, facilitate resource allocation, and improve patient clinical outcomes to prevent long COVID incidence.
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Ghimire et al. (2023) studied this question.
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