Oxidative Stress and Nrf2-Mediated Cellular Inflammation
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: 30 July 2024 | Viewed by 1394
Special Issue Editors
Interests: mesenchymal stem cell differentiation; biomaterials; tissue regeneration; hyaluronic acid; histology
Special Issues, Collections and Topics in MDPI journals
Interests: inflammation; hyaluronic acid; biomaterials; oxidative stress; tendons
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Nuclear factor erythroid 2‐related factor 2 (NRF2) is a master transcriptional regulator of genes whose products defend our cells from toxic and oxidative insults. NRF2 can influence several cellular functions as it is located at the intersection of crucial signaling pathways in the maintenance of the intracellular redox balance, including cellular metabolism, proteostasis, mitochondrial function and inflammation. Oxidative stress boosts NRF2 activation and links NRF2 with the activation of inflammasomes. Failure in NRF2 activation or its degradation leads to increased inflammation and the secretion of pro-inflammatory cytokines. Exaggerated inflammation negatively evolves into apoptosis/pyroptosis.
In recent decades, a plethora of literature has focused on the investigation of NRF2 modulation for therapeutic purposes, which requires accurate knowledge of the cell context and the specific timeframe both of NRF2 activation and inhibition. This Special Issue offers an overview on the most recent findings regarding the involvement of NRF2 in the modulation of cellular inflammation at a molecular level.
Prof. Dr. Amelia Cataldi
Dr. Marialucia Gallorini
Guest Editors
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Keywords
- Nrf2
- oxidative stress
- cell signaling
- inflammation