Cited by 239Genomics, phytochemicals, and oxidative stressRedox biology and oxidative stressNF-κB Signaling Pathways

Redox activation of Nrf2 & NF-κB: A double end sword?

Buelna-Chontal, Mabel, Zazueta, Cecilia·2013·Cellular Signalling

Abstract

Moderate concentrations of reactive oxygen species (ROS) are produced by diverse sources under physiological conditions. At such low levels, these molecules may act as upstream mediators of relevant signaling pathways; however an increase in their concentration with respect to the antioxidant system activity, changes their redox signaling function into a deleterious role. Thus, cell health depends, at least in part, on redox balance. This review includes global aspects of oxygen chemistry, ROS generation, antioxidant system, and redox signaling. It is also focused on the description of two relevant redox-sensitive transcription factors: nuclear factor erythroid 2-related factor 2 (Nrf2), which may be a potential target to confer cell protection, and nuclear factor κB (NF-κB), which is involved in deleterious effects in the cell. Finally, recent findings on the interplay between both factors for the development of different pathologies are discussed.

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Crossref · 10.1016/j.cellsig.2013.08.007

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121 of 121 references verified0 citation errors · 0 not checkable

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  • The interplay between oxidative stress and inflammation is partly governed by reciprocal interactions between the transcription factors Nrf2 and NF-kB.

    “The complex interplay between oxidative stress and inflammation is in part governed by the reciprocal interactions between the transcription factors Nrf2 (whose nuclear translocation induces antioxidant phase II gene transcription) and NF-kB (whose translocation to the nucleus promotes transcription of many pro-inflammatory genes) (Buelna-Chontal and Zazueta, 2013).”
  • Disruption of NFE2L2 induces NF-κB activation, probably by modifying NFKB1A degradation and NF-κB binding to DNA.

    “At the molecular level, the antagonism between antioxidant-promoting NFE2L2 and inflammatory gene-regulating NF-κB may control the balance between oxidative stress and inflammation 94 : disruption of NFE2L2 induces NF-κB activation, probably by modifying NF-κB inhibitor α (NFKB1A, also known as IkBα) degradation and NF-κB binding to DNA 95,96”

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Authors
Buelna-Chontal, M., & Zazueta, C.
Affiliations
Instituto Nacional de Cardiología (MX)
Corresponding author
Zazueta, Cecilia
Venue
Cellular Signalling
Publisher
Elsevier BV
Published
2013-12
Volume
25
Issue
12
Pages
2548-2557
ISSN
0898-6568 (ISSN-L)
OpenAlex
W2058792844
Cited by
239
References
121
Citations by year
2026: 9 · 2025: 12 · 2024: 6 · 2023: 12 · 2022: 14 · 2021: 27 · 2020: 21 · 2019: 22 · 2018: 31 · 2017: 26 · 2016: 20 · 2015: 25 · 2014: 13 · 2013: 1
FWCI
1.85
Type
journal article
Language
en
Open access
closed
Locations
  • Cellular Signalling (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Council of Science and Technology (CONACyT), Mexico (177527)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
Nrf2, NF-κB, reactive oxygen species, redox signaling, redox homeostasis, antioxidant defense, oxidative stress, transcription factors, cytoprotection, oxygen chemistry
MeSH terms
Animals, Humans, Oxidation-Reduction, Signal Transduction, NF-kappa B, Reactive Oxygen Species, NF-E2-Related Factor 2

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