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Review
. 2020 Dec;85(12):1543-1553.
doi: 10.1134/S0006297920120068.

COVID-19 and Oxidative Stress

B V Chernyak  1 , E N Popova  1 , A S Prikhodko  1   2 , O A Grebenchikov  3 , L A Zinovkina  2 , R A Zinovkin  4   5   6
Affiliations
Review

COVID-19 and Oxidative Stress

B V Chernyak et al. Biochemistry (Mosc). 2020 Dec.

Abstract

Pathogenesis of the novel coronavirus infection COVID-19 is the subject of active research around the world. COVID-19 caused by the SARS-CoV-2 is a complex disease in which interaction of the virus with target cells, action of the immune system and the body's systemic response to these events are closely intertwined. Many respiratory viral infections, including COVID-19, cause death of the infected cells, activation of innate immune response, and secretion of inflammatory cytokines. All these processes are associated with the development of oxidative stress, which makes an important contribution to pathogenesis of the viral infections. This review analyzes information on the oxidative stress associated with the infections caused by SARS-CoV-2 and other respiratory viruses. The review also focuses on involvement of the vascular endothelium in the COVID-19 pathogenesis.

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Conflict of interest statement

The authors declare no conflict of interest in financial or any other sphere. This article does not contain any studies with human participants or animals performed by any of the authors.

Figures

Figure.
Figure.
Angiotensin II (ATII) interacts with AT1R receptor and induces ROS production via NADPH oxidase (NOX) in endothelial cells triggering mitochondrial oxidative stress and endothelial dysfunction. It is believed that SARS-CoV-2 S-protein binds to ACE2 causing its subsequent local or systemic depletion of this enzyme that cleaves ATII, which, in turn, increased ATII level.
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