Nrf2, the Master Regulator of Anti-Oxidative Responses
Open accessAbstract
Tight regulation of inflammation is very important to guarantee a balanced immune response without developing chronic inflammation. One of the major mediators of the resolution of inflammation is the transcription factor: the nuclear factor erythroid 2-like 2 (Nrf2). Stabilized following oxidative stress, Nrf2 induces the expression of antioxidants as well as cytoprotective genes, which provoke an anti-inflammatory expression profile, and is crucial for the initiation of healing. In view of this fundamental modulatory role, it is clear that both hyper- or hypoactivation of Nrf2 contribute to the onset of chronic diseases. Understanding the tight regulation of Nrf2 expression/activation and its interaction with signaling pathways, known to affect inflammatory processes, will facilitate development of therapeutic approaches to prevent Nrf2 dysregulation and ameliorate chronic inflammatory diseases. We discuss in this review the principle mechanisms of Nrf2 regulation with a focus on inflammation and autophagy, extending the role of dysregulated Nrf2 to chronic diseases and tumor development.
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Nrf2 encodes a transcription factor responsible for activating the expression of protective enzymes.
“We also noted that the expression of Nrf2, which encodes a transcription factor responsible for activating the expression of protective enzymes, was upregulated [44].”
From Dyslipidemia-Induced Mitochondrial Dysfunctions in the Brains Does Not Reach Pathological Levels in the ApoE-Knockout Mice (2026) · cites this paper as [44]
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- Authors
- Vomund, S., Schäfer, A., Parnham, M., Brüne, B., & Von Knethen, A.
- Affiliations
- Fraunhofer Institute for Molecular Biology and Applied Ecology (DE)
- Goethe University Frankfurt (DE)
- Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Project Group Translational Medicine & Pharmacology TMP, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2017-12-20
- Volume
- 18
- Issue
- 12
- Pages
- 2772
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC5751370
- OpenAlex
- W2779339038
- Cited by
- 752
- References
- 19
- Citations by year
- 2026: 94 · 2025: 84 · 2024: 115 · 2023: 92 · 2022: 95 · 2021: 106 · 2020: 92 · 2019: 56 · 2018: 17
- FWCI
- 4.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Publikationsdatenbank der Fraunhofer-Gesellschaft (Fraunhofer-Gesellschaft) (submittedVersion, other-oa)
- Fraunhofer-Publica (Fraunhofer-Gesellschaft) (submittedVersion)
- Publication Server of Goethe University Frankfurt am Main (Goethe University Frankfurt) (submittedVersion, cc-by)
- Funders
- Spinal Muscular Atrophy Foundation
- Deutsche Forschungsgemeinschaft (SFB 815, KN493/9-2)
- Else Kröner-Fresenius-Stiftung (SFB815)
- Institut National d'assurance Maladie-Invalidité
- 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, oxidative stress, antioxidant response, inflammation, chronic inflammation, autophagy, transcription factor regulation, chronic disease, carcinogenesis, cytoprotective genes, inflammation resolution
- MeSH terms
- Animals, Antioxidants, Autophagy, Humans, Mitochondria, Oxidative Stress, NF-E2-Related Factor 2
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