SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Hamad R.S.; Al-kuraishy H.M.; Alexiou A.; Papadakis M.; Ahmed E.A.; Saad H.M.; Batiha G.E.-S.

Journal: Cell Stress and Chaperones

Publisher: Springer Science and Business Media B.V.

Publication Date: November 2023

Volume / Issue: Volume 28 / Issue 6

Pages: 657–673

ISSN: 13558145

DOI: 10.1007/s12192-023-01379-0

Scopus: View on Scopus

PubMed: 37796433

Document Type: Short survey

Access: All Open Access; Green Open Access; Hybrid Gold Open Access


Authors and Affiliations

Hamad R.S., Biological Sciences Department, College of Science, King Faisal University, Al Ahsa, 31982, Saudi Arabia, Central Laboratory, Theodor Bilharz Research Institute, Giza, 12411, Egypt; Al-kuraishy H.M., Department of Pharmacology, Toxicology and Medicine, Medical Faculty, College of Medicine, Al-Mustansiriyah University, P.O. Box 14132, Baghdad, Iraq; Alexiou A., Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, 2770, NSW, Australia, AFNP Med, Vienna, 1030, Austria; Papadakis M., Department of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Heusnerstrasse 40, Wuppertal, 42283, Germany; Ahmed E.A., Department of Pharmacology, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, 41522, Egypt; Saad H.M., Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, 51744, Egypt; Batiha G.E.-S., Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, Egypt


Abstract

Coronavirus disease 2019 (COVID-19) is a recent pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) leading to pulmonary and extra-pulmonary manifestations due to the development of oxidative stress (OS) and hyperinflammation. The underlying cause for OS and hyperinflammation in COVID-19 may be related to the inhibition of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of antioxidative responses and cellular homeostasis. The Nrf2 pathway inhibits the expression of pro-inflammatory cytokines and the development of cytokine storm and OS in COVID-19. Nrf2 activators can attenuate endothelial dysfunction (ED), renin-angiotensin system (RAS) dysregulation, immune thrombosis, and coagulopathy. Hence, this review aimed to reveal the potential role of the Nrf2 pathway and its activators in the management of COVID-19. As well, we tried to revise the mechanistic role of the Nrf2 pathway in COVID-19. © 2023, The Author(s).


Keywords

COVID-19; Nuclear factor erythroid 2-related factor 2; Oxidative stress; SARS-CoV-2; Humans; Lung; NF-E2-Related Factor 2; Renin-Angiotensin System; advanced glycation end product; angiotensin converting enzyme 2; antioxidant; beta transducin repeat containing protein; cytokine; heme oxygenase 1; high mobility box protein 1; inflammasome; kelch like ECH associated protein 1; mammalian target of rapamycin; membrane protein; metalloproteinase; nucleotide binding oligomerization domain like receptor; oxidoreductase; protein kinase; quinone derivative; STAT3 protein; toll like receptor; toll like receptor 4; transcription factor Maf; transcription factor Nrf2; unclassified drug; antiinflammatory activity; antioxidant activity; antioxidant responsive element; blood clotting disorder; coronavirus disease 2019; cytokine storm; cytoplasm; endothelial dysfunction; essential gene; gene expression; homeostasis; human; hyperinflammation; immune dysregulation; Nrf2 signaling; pandemic; Pi3K/Akt signaling; protein expression; protein function; renin angiotensin aldosterone system; Severe acute respiratory syndrome coronavirus 2; Short Survey; signal transduction; thrombosis


Citation Information

Scopus Citations: 22


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