Special Issue "Role of Nrf2 in Disease: Novel Molecular Mechanisms and Therapeutic Approaches"
Deadline for manuscript submissions: closed (31 August 2020).
Interests: inflammation; autophagy; proteasome; proteostasis; oxidative stress; neurodegeneration; KEAP1; metabolism; redox balance
Special Issues and Collections in MDPI journals
Since it was cloned and characterized, the transcription factor (nuclear factor erythroid-2-related factor 2) NRF2 has been implicated in processes associated with redox balance, inflammation, proteostasis and lipids, purines and pentoses metabolism, becoming a pleiotropic transcription factor. For this reason, NRF2 has developed as a polyvalent target against various pathologies, where the signaling system of NRF2 is altered. Under normal conditions, basal NRF2 levels are low due to its interaction to KEAP1 (Kelch-like ECH-associated protein 1) that binds to and negatively regulates NRF2. Electrophiles or oxidative stress induce the inactivation of KEAP1 by direct modification of reactive cysteine residues, leading to the release and stabilization of NRF2, that translocates to the nucleus to bind to the antioxidant response element (ARE) sequence in the promoter regions of NRF2-dependent genes. This system makes it a good pharmacological target to modulate the activation of NRF2 and, therefore, its application in various pathologies.
This Special Issue on NRF2 should, on one hand, emphasize the importance of this transcription factor, and, on the other hand, it should also highlight existing pharmacological components that can modify the NRF2 signaling pathway. In this regard, we would like to invite review articles which address the above-mentioned issues from different perspectives. Alternatively, any original research papers contributing significantly to NRF2 signaling progress or advancing our understanding of biological implications are highly welcome. We look forward to reading your contributions.
Prof. Isabel Lastres-Becker
Manuscript Submission Information
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- oxidative stress
- redox balance