Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 18, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/ijms18122772
Keywords
Nrf2; electrophiles; reactive oxygen species; transcription factor; antioxidants
Funding
- Deutsche Forschungsgemeinschaft [KN493/9-2, KN493/11-1, SFB815 TP3, SFB815 TP8]
- Else Kroner-Fresenius Foundation (EKFS), Research Training Group Translational Research Innovation-Pharma (TRIP)
- Landesoffensive zur Entwicklung wissenschaftlich-okonomischer Exzellenz (LOEWE), Schwerpunkt Anwendungsorientierte Arzneimittelforschung
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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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