Cited by 1,200Genomics, phytochemicals, and oxidative stressNF-κB Signaling PathwaysRedox biology and oxidative stress

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Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways

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Wardyn, Joanna D., Ponsford, Amy H., Sanderson, Christopher M.·2015·Biochemical Society Transactions

DOI 10.1042/bst20150014PMC PMC4613495

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Abstract

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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1 retracted

Src Subfamily Kinases Regulate Nuclear Export and Degradation of Transcription Factor Nrf2 to Switch Off Nrf2-mediated Antioxidant Activation of Cytoprotective Gene Expression
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p62/SQSTM1 Is a Target Gene for Transcription Factor NRF2 and Creates a Positive Feedback Loop by Inducing Antioxidant Response Element-driven Gene Transcription
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“Remarkably, the absence of Nrf2 has been observed to exacerbate NF-j B activity, culminating in heightened release of inflammatory cytokines 30,31 .”
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“Conversely, inactivation of Nrf2 reduces NF-κB suppression, thereby exacerbating the inflammatory response [53].”
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Background
Novel Series of Dual NRF2 Inducers and Selective MAO-B Inhibitors for the Treatment of Parkinson’s Disease
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“In general, NRF2 pathway activation decreases NF-κB response [84].”
Background
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“Meanwhile, accumulated evidence indicates that the Nuclear factor-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, a major antioxidant defense system, regulates inflammatory responses by suppressing the excessive production of ROS, inflammatory mediates, and pro-inflammatory cytokines [35].”
Background
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“In this regard, the diminished cellular Nrf2 has been associated with enhanced NF-κB transcriptional activity, culminating in overshooting of pro-inflammatory cytokines [48].”
Background
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“Maintaining an appropriate metabolic interaction between Nrf2 and NF-κB after irradiation with UV rays also influences metabolic homeostasis [8,60].”
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Background
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Background
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Background
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BackgroundInfluential
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Background
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Background
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“Then, Nrf2 associates with antioxidant response elements (AREs) and triggers the transcription and expression of a series of Nrf2-dependent genes [10, 11], including heme oxygenase 1 (HO1), NAD (P) H quinone oxidoreductase-1 (NQO1), and γ-glutamyl cysteine ligase catalytic subunit (GCLC), and all of them exhibit robus…”
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Joint Transcriptome and Metabolome Analysis Prevails the Biological Mechanisms Underlying the Pro-Survival Fight in In Vitro Heat-Stressed Granulosa Cells
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“Nrf2 and NF-κB pathways are supportive and sometimes antagonistic to bringing up cellular homeostasis in the event of stress; NF-κB promotes inflammation and inflammation and subsequently promotes transcription activities related to energetic catabolic support [44].”
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“Nrf2 is a major regulator that regulates redox homeostasis, and HO-1 is a target gene that is pivotal to Nrf2-mediated NF-κB inhibition [45].”
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“Moreover, there is an important crosstalk between Nfkb and Nrf2 pathways (Chen et al., 2021; Wardyn et al., 2015).”
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“Furthermore, S. platensis inhibit the expression of TLR4, MyD88, and NF-κB in the colon of HFD-fed rats, explaining the reduction in serum levels of the products of this pathway, such as TNF-α and IL-6 (Yu et al. 2020).”
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Authors: Wardyn, J. D., Ponsford, A. H., & Sanderson, C. M.
Affiliations: University of Liverpool (GB)
Corresponding author: Sanderson, Christopher M.
ORCID: Ponsford, Amy H.
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
DOI: 10.1042/bst20150014
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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Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways

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