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Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways
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In most tissues, cells are exposed to frequent changes in levels of oxidative stress and inflammation. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and nuclear factor-κB (NF-κB) are the two key transcription factors that regulate cellular responses to oxidative stress and inflammation respectively. Pharmacological and genetic studies suggest that there is functional cross-talk between these two important pathways. The absence of Nrf2 can exacerbate NF-κB activity leading to increased cytokine production, whereas NF-κB can modulate Nrf2 transcription and activity, having both positive and negative effects on the target gene expression. This review focuses on the potentially complex molecular mechanisms that link the Nrf2 and NF-κB pathways and the importance of designing more effective therapeutic strategies to prevent or treat a broad range of neurological disorders.
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“Lack of Nrf2 activity can exacerbate NF-κB signaling, leading to increased cytokine production; alternatively, NF-κB can modulate Nrf2 activity, having both positive and negative effects on target gene expression [152, 153].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [152]
In the citing paper
“Competition of Nrf2 and NF-κB at DNA binding level is one of the anti-inflammatory mechanisms of Nrf2 (60, 61).”
From Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway (2019) · cites this paper as [60]
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“The interplay between NF-κ B, MAPK, and Nrf2 may provide an additional layer of protection by refining and enhancing cellular adaptive responses to oxidative challenges (Zhou et al., 2018; Wardyn et al., 2015).”
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“This reasoning behind the spike in HO-1 gene expression by CNDs is still unclear, but the Nrf2 pathway could explain the change [27,67].”
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Metadata
- Authors
- Wardyn, J. D., Ponsford, A. H., & Sanderson, C. M.
- Affiliations
- University of Liverpool (GB)
- Corresponding author
- Sanderson, Christopher M.
- Venue
- Biochemical Society Transactions
- Publisher
- Portland Press Ltd.
- Published
- 2015-08-01
- Volume
- 43
- Issue
- 4
- Pages
- 621-626
- ISSN
- 0300-5127 (ISSN-L)
- 1470-8752
- PMC
- PMC4613495
- OpenAlex
- W2133584350
- Cited by
- 1,200
- References
- 53
- Citations by year
- 2026: 139 · 2025: 131 · 2024: 117 · 2023: 145 · 2022: 165 · 2021: 154 · 2020: 124 · 2019: 95 · 2018: 68 · 2017: 44 · 2016: 15 · 2015: 1
- FWCI
- 4.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Society Transactions (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (096564/Z/11/Z)
- Directorate for Biological Sciences
- Biotechnology and Biological Sciences Research Council (1222890, BB/J014516/1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- Nrf2, NF-κB, oxidative stress, inflammation, cytokine production, neurological disorders, treatment options
- MeSH terms
- Animals, Gene Expression Regulation, Humans, Nervous System Diseases, Signal Transduction, Cytokines, NF-kappa B, Oxidative Stress, NF-E2-Related Factor 2
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