Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients

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R. A. Zinovkin^1,2,3,a* and O. A. Grebenchikov⁴

¹Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia

²Institute of Mitoengineering, Lomonosov Moscow State University, 119992 Moscow, Russia

³Institute of Molecular Medicine, Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia

⁴Negovsky Research Institute of General Reanimatology, Russian Academy of Medical Sciences, 107031 Moscow, Russia

^* To whom correspondence should be addressed.

Received May 30, 2020; Revised June 4, 2020; Accepted June 4, 2020

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Nrf2 is a key transcription factor responsible for antioxidant defense in many tissues and cells, including alveolar epithelium, endothelium, and macrophages. Furthermore, Nrf2 functions as a transcriptional repressor that inhibits expression of the inflammatory cytokines in macrophages. Critically ill patients with COVID-19 infection often present signs of high oxidative stress and systemic inflammation – the leading causes of mortality. This article suggests rationale for the use of Nrf2 inducers to prevent development of an excessive inflammatory response in COVID-19 patients.

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KEY WORDS: Nrf2, SARS-CoV-2, COVID-19, cytokine storm, oxidative stress

DOI: 10.1134/S0006297920070111

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