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Nrf2 promotes survival following exposure to ionizing radiation
Open accessAbstract
Nrf2 is a transcription factor that promotes antioxidant and drug-metabolizing gene expression. It also regulates the transcription of genes involved in carbohydrate and lipid metabolism, NADPH regeneration, and heme and iron metabolism, as well as proteasome metabolism. Emerging research has identified Nrf2 as a critical factor for promoting survival of mammalian cells subjected to ionizing radiation. At a mechanistic level, Nrf2 promotes the repair of DNA damage and drives detoxification of superoxide that is generated hours to days after irradiation. This review summarizes research in these areas and discusses targeting of Nrf2 in radiation-resistant cancer and Nrf2׳s role in mitigating acute radiation syndrome.
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“equol itself is a very strong antioxidant, and, in turn, it can increase the levels of the master gene, Nrf2, which regulates the endogenous expression of detoxifying proteins and many other antioxidant enzymes that are involved in wound repair, protection against skin cancer”
From Equol’s Anti-Aging Effects Protect against Environmental Assaults by Increasing Skin Antioxidant Defense and ECM Proteins While Decreasing Oxidative Stress and Inflammation (2018) · cites this paper as [72]
Experimental — accuracy not yet measuredIn the citing paper
“Nrf2 plays a key role in the cellular defense against oxidative and xenobiotic stressors by its capacity to induce the expression of numerous genes, which encode detoxifying enzymes and antioxidant proteins that provide protection in endothelial cells, skin morphogenesis, wound repair, and skin cancer [70][71][72][73].”
In the citing paper
“where Nrf2 activation guards against dermal damage, from sunlight (ionizing radiation) and oxidative stress via ROS [2,69-73,76,99].”
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Metadata
- Authors
- Sekhar, K. R., & Freeman, M. L.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Freeman, Michael L.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 88
- Issue
- Pt B
- Pages
- 268-274
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC4628893
- OpenAlex
- W767415338
- Cited by
- 109
- References
- 91
- Citations by year
- 2026: 5 · 2025: 14 · 2024: 9 · 2023: 12 · 2022: 6 · 2021: 15 · 2020: 16 · 2019: 3 · 2018: 10 · 2017: 12 · 2016: 4 · 2015: 3
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH/NHLBI (RO1HL112286)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- Nrf2, ionizing radiation, radioresistance (biology), DNA repair, superoxide detoxification, antioxidant gene expression, radiation sickness, cell survival
- MeSH terms
- Animals, Cell Survival, DNA Repair, Humans, Radiation Tolerance, Radiation, Ionizing, NF-E2-Related Factor 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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