GPX4
细胞生物学
细胞内
脂质过氧化
转录因子
细胞
程序性细胞死亡
机制(生物学)
癌细胞
生物
信号转导
化学
氧化应激
生物化学
细胞凋亡
癌症
基因
谷胱甘肽过氧化物酶
遗传学
超氧化物歧化酶
哲学
认识论
作者
Hironari Nishizawa,Mie Yamanaka,Kazuhiko Igarashi
出处
期刊:FEBS Journal
[Wiley]
日期:2022-02-17
卷期号:290 (7): 1688-1704
被引量:41
摘要
Ferroptosis is triggered by a chain of intracellular labile iron-dependent peroxidation of cell membrane phospholipids. Ferroptosis is important not only as a cause of ischaemic and neurodegenerative diseases but also as a mechanism of cancer suppression, and a better understanding of its regulatory mechanism is required. It has become clear that ferroptosis is finely controlled by two oxidative stress-responsive transcription factors, NRF2 (NF-E2-related factor 2) and BACH1 (BTB and CNC homology 1). NRF2 and BACH1 inhibit and promote ferroptosis, respectively, by activating or suppressing the expression of genes in the major regulatory pathways of ferroptosis: intracellular labile iron metabolism, the GSH (glutathione) -GPX4 (glutathione peroxidase 4) pathway and the FSP1 (ferroptosis suppressor protein 1)-CoQ (coenzyme Q) pathway. In addition to this, NRF2 and BACH1 control ferroptosis through the regulation of lipid metabolism and cell differentiation. This multifaceted regulation of ferroptosis by NRF2 and BACH1 is considered to have been acquired during the evolution of multicellular organisms, allowing the utilization of ferroptosis for maintaining homeostasis, including cancer suppression. In terms of cell-cell interaction, it has been revealed that ferroptosis has the property of propagating to surrounding cells along with lipid peroxidation. The regulation of ferroptosis by NRF2 and BACH1 and the propagation phenomenon could be used to realize anticancer cell therapy in the future. In this review, these points will be summarized and discussed.
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