Review
Version 1
Preserved in Portico This version is not peer-reviewed
NRF2, a Superstar in Ferroptosis
Version 1
: Received: 21 August 2023 / Approved: 22 August 2023 / Online: 23 August 2023 (03:28:45 CEST)
A peer-reviewed article of this Preprint also exists.
Yan, R.; Lin, B.; Jin, W.; Tang, L.; Hu, S.; Cai, R. NRF2, a Superstar of Ferroptosis. Antioxidants 2023, 12, 1739. Yan, R.; Lin, B.; Jin, W.; Tang, L.; Hu, S.; Cai, R. NRF2, a Superstar of Ferroptosis. Antioxidants 2023, 12, 1739.
Abstract
Ferroptosis is an iron-dependent and lipid peroxidation-driven cell death cascade, occurring when there is an imbalance of redox homeostasis in the cell. Nuclear factor E2 related factor 2 (NFE2L2, also known as NRF2) is key for cellular antioxidant responses, which promotes downstream gene transcription by binding to their antioxidant response elements (AREs). Numerous studies suggest that NRF2 assumes an extremely important role in the regulation of ferroptosis, for its various functions on iron, lipid and amino acid metabolism and so on. Many pathological states are relevant to ferroptosis. In cancer cells, ferroptosis is frequently found abnormal suppression. While during tissue damages, ferroptosis is recurrently promoted, resulting in a large number of cell deaths and ultimately loss of the functions of the corresponding organs. Therefore, targeting NRF2-related signaling pathways, to induce or inhibit ferroptosis, has become a great potential therapy for combating cancers, as well as preventing neurodegenerative and ischemic diseases. In this review, a brief overview of the research process of ferroptosis over the past decade will be presented. In particular, the mechanisms of ferroptosis and a focus on the regulation of ferroptosis by NRF2 will be discussed. Finally, the review will briefly list some clinical applications of targeting the NRF2 signaling pathway in the treatment of diseases.
Keywords
NRF2; ferroptosis; antioxidant; metabolism
Subject
Biology and Life Sciences, Cell and Developmental Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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