Dr Paul Hiebert P.Hiebert@hull.ac.uk
Lecturer in Wound Healing
Targeting NRF2 to promote epithelial repair
Hiebert, Paul; Werner, Sabine
Authors
Sabine Werner
Abstract
The transcription factor NRF2 is well known as a master regulator of the cellular stress response. As such, activation of NRF2 has gained widespread attention for its potential to prevent tissue injury, but also as a possible therapeutic approach to promote repair processes. While NRF2 activation affects most or even all cell types, its effect on epithelial cells during repair processes has been particularly well studied. In response to tissue injury, these cells proliferate, migrate and/or spread to effectively repair the damage. In this review, we discuss how NRF2 governs repair of epithelial tissues, and we highlight the increasing number of NRF2 targets with diverse roles in regulating epithelial repair.
Citation
Hiebert, P., & Werner, S. (2023). Targeting NRF2 to promote epithelial repair. Biochemical Society Transactions, 51(1), 101-111. https://doi.org/10.1042/BST20220228
Journal Article Type | Review |
---|---|
Acceptance Date | Jan 20, 2023 |
Online Publication Date | Feb 10, 2023 |
Publication Date | Feb 1, 2023 |
Deposit Date | Feb 14, 2024 |
Publicly Available Date | Feb 16, 2024 |
Journal | Biochemical Society Transactions |
Print ISSN | 0300-5127 |
Electronic ISSN | 1470-8752 |
Publisher | Portland Press |
Peer Reviewed | Peer Reviewed |
Volume | 51 |
Issue | 1 |
Pages | 101-111 |
DOI | https://doi.org/10.1042/BST20220228 |
Keywords | Cell proliferation; Cytoprotection; Keap1; NRF2; Tissue repair; Wound healing |
Public URL | https://hull-repository.worktribe.com/output/4547451 |
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Copyright Statement
© 2023 The Author(s)
This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND). Open access for this article was enabled by the participation of ETH Zurich in an all-inclusive Read & Publish agreement with Portland Press and the Biochemical Society.
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