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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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BackgroundKeap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex
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Self-citation
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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