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자료유형
학술저널
저자정보
Donna D. Zhang (College of Pharmacy University of Arizona) Aryatara Shakya (College of Pharmacy University of Arizona) Nicholas W. McKee (College of Pharmacy University of Arizona) Matthew Dodson (College of Pharmacy University of Arizona) Eli Chapman (College of Pharmacy University of Arizona)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제46권 제3호
발행연도
2023.3
수록면
165 - 175 (11page)
DOI
10.14348/molcells.2023.2196

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The transcription factor Nrf2 was originally identified as a master regulator of redox homeostasis, as it governs the expression of a battery of genes involved in mitigating oxidative and electrophilic stress. However, the central role of Nrf2 in dictating multiple facets of the cellular stress response has defined the Nrf2 pathway as a general mediator of cell survival. Recent studies have indicated that Nrf2 regulates the expression of genes controlling ferroptosis, an ironand lipid peroxidation-dependent form of cell death. While Nrf2 was initially thought to have anti-ferroptotic function primarily through regulation of the antioxidant response, accumulating evidence has indicated that Nrf2 also exerts anti-ferroptotic effects via regulation of key aspects of iron and lipid metabolism. In this review, we will explore the emerging role of Nrf2 in mediating iron homeostasis and lipid peroxidation, where several Nrf2 target genes have been identified that encode critical proteins involved in these pathways. A better understanding of the mechanistic relationship between Nrf2 and ferroptosis, including how genetic and/or pharmacological manipulation of Nrf2 affect the ferroptotic response, should facilitate the development of new therapies that can be used to treat ferroptosis-associated diseases.

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