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Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients
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...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Pleiades Publishing
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7356136/ https://www.ncbi.nlm.nih.gov/pubmed/33040727 http://dx.doi.org/10.1134/S0006297920070111 |
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author | Zinovkin, R. A. Grebenchikov, O. A. |
author_facet | Zinovkin, R. A. Grebenchikov, O. A. |
author_sort | Zinovkin, R. A. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7356136 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Pleiades Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-73561362020-07-13 Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients Zinovkin, R. A. Grebenchikov, O. A. Biochemistry (Mosc) Hypothesis 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. Pleiades Publishing 2020-07-13 2020 /pmc/articles/PMC7356136/ /pubmed/33040727 http://dx.doi.org/10.1134/S0006297920070111 Text en © Pleiades Publishing, Ltd. 2020 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Hypothesis Zinovkin, R. A. Grebenchikov, O. A. Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title | Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title_full | Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title_fullStr | Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title_full_unstemmed | Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title_short | Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients |
title_sort | transcription factor nrf2 as a potential therapeutic target for prevention of cytokine storm in covid-19 patients |
topic | Hypothesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7356136/ https://www.ncbi.nlm.nih.gov/pubmed/33040727 http://dx.doi.org/10.1134/S0006297920070111 |
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