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Activation of Nrf2-antioxidant signaling attenuates NFκB-inflammatory response and elicits apoptosis
Open accessAbstract
Oxidative stress has been implicated in the etiology of neurodegenerative disease, cancer and aging. Indeed, accumulation of reactive oxygen and nitrogen species generated by inflammatory cells that created oxidative stress is thought to be one of the major factor by which chronic inflammation contributes to neoplastic transformation as well as many other diseases. We have recently reported that mice lacking nuclear factor-erythroid 2-related factor 2 (Nrf2) are more susceptible to dextran sulfate sodium (DSS)-induced colitis and colorectal carcinogenesis. Nrf2 is a basic leucine zipper redox-sensitive transcriptional factor that plays a center role in ARE (antioxidant response element)-mediated induction of phase II detoxifying and antioxidant enzymes. We found that increased susceptibility of Nrf2 deficient mice to DSS-induced colitis and colorectal cancer was associated with decreased expression of antioxidant/phase II detoxifying enzymes in parallel with upregulation of pro-inflammatory cytokines/biomarkers. These findings suggest that Nrf2 may play an important role in defense against oxidative stress possibly by activation of cellular antioxidant machinery as well as suppression of pro-inflammatory signaling pathways. In addition, in vivo and in vitro data generated from our laboratory suggest that many dietary compounds can differentially regulate Nrf2-mediated antioxidant/anti-inflammatory signaling pathways as the first line defense or induce apoptosis once the cells have been damaged. In this review, we will summarize our thoughts on the potential cross-talks between Nrf2 and NFkappaB pathways. Although the mechanisms involved in the cross-talk between these signaling pathways are still illusive, targeting Nrf2-antioxidative stress signaling is an ideal strategy to prevent or treat oxidative stress-related diseases.
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“The anti-inflammatory role of Nrf2 also includes Nrf2-mediated inhibition of the pro-inflammatory NF-ΚB pathway and inhibition of expression of pro-inflammatory cytokines [195,196,197].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [196]
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Nrf2–Keap1 defines a physiologically important stress response mechanism
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“enhancer called antioxidant response element (ARE), and eventually recruits the whole transcription machinery including the RNA polymerase II to transcribe phase II/III genes [1].”
BackgroundKeap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex
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“, a high affinity phase I binding, mediated by the ETGE motif and a low affinity phase II binding mediated by the DLG motif, has been distinguished [8].”
BackgroundStructural basis for defects of Keap1 activity provoked by its point mutations in lung cancer
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“The geometric distance between the two Kelch domains matches perfectly with the length of this alpha helix [10].”
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BackgroundInfluentialNrf2-Deficient Mice Have an Increased Susceptibility to Dextran Sulfate Sodium–Induced Colitis
Khor, T. O., Huang, M., Kwon, K. H., Chan, J. Y., Reddy, B. S., & Kong, A. T. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-3562 · Cited by 530
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Identification of the interactive interface and phylogenic conservation of the Nrf2‐Keap1 system
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Self-citationNrf2 Possesses a Redox-sensitive Nuclear Exporting Signal in the Neh5 Transactivation Domain
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Nrf2 Possesses a Redox-insensitive Nuclear Export Signal Overlapping with the Leucine Zipper Motif
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Role of nrf2 in oxidative stress and toxicity
Ma, Q. (2013) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-011112-140320 · Cited by 4,903
The NLRP3 inflammasome: molecular activation and regulation to therapeutics
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Nrf2-Keap1 signaling in oxidative and reductive stress
Bellezza, I., Giambanco, I., Minelli, A., & Donato, R. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2018.02.010 · Cited by 2,134
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An Overview of Nrf2 Signaling Pathway and Its Role in Inflammation
Saha, S., Buttari, B., Panieri, E., Profumo, E., & Saso, L. (2020) · Molecules · doi:10.3390/molecules25225474 · Cited by 1,460
Metadata
- Authors
- Li, W., Khor, T. O., Xu, C., Shen, G., Jeong, W.-S., Yu, S., & Kong, A.-N.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Kong, Ah-Ng
- Venue
- Biochemical Pharmacology
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 76
- Issue
- 11
- Pages
- 1485-1489
- ISSN
- 0006-2952 (ISSN-L)
- PMC
- PMC2610259
- OpenAlex
- W2064452102
- Cited by
- 738
- References
- 25
- Citations by year
- 2026: 17 · 2025: 32 · 2024: 28 · 2023: 43 · 2022: 66 · 2021: 59 · 2020: 52 · 2019: 58 · 2018: 58 · 2017: 43 · 2016: 52 · 2015: 52 · 2014: 29 · 2013: 48 · 2012: 33
- FWCI
- 9.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA118947, CA094828, R01CA073674, CA-118947, CA073674, R01CA094828)
- National Institute of Environmental Health Sciences (P30ES005022)
- 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, antioxidant response element, phase II enzymes, colitis, colorectal cancer, inflammatory cytokines, apoptosis, dietary compounds, chronic inflammation, neurodegenerative diseases, aging
- MeSH terms
- Animals, Antioxidants, Signal Transduction, NF-kappa B, Apoptosis, Oxidative Stress, Inflammation Mediators, NF-E2-Related Factor 2, Mice
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