KEAP1型
信号转导
细胞生物学
氧化应激
程序性细胞死亡
缺氧(环境)
脂质过氧化
GPX4
活性氧
生物
化学
细胞凋亡
生物化学
转录因子
氧气
超氧化物歧化酶
基因
有机化学
谷胱甘肽过氧化物酶
作者
Xīn Gào,Wei Hu,Dianlun Qian,Xiangfeng Bai,Huilin He,Lin Li,Shibo Sun
标识
DOI:10.1007/s10571-023-01388-8
摘要
Abstract Ferroptosis is a new form of programmed cell death, which is characterized by the iron-dependent accumulation of lipid peroxidation and increase of ROS, resulting in oxidative stress and cell death. Iron, lipid, and multiple signaling pathways precisely control the occurrence and implementation of ferroptosis. The pathways mainly include Nrf2/HO-1 signaling pathway, p62/Keap1/Nrf2 signaling pathway. Activating p62/Keap1/Nrf2 signaling pathway inhibits ferroptosis. Nrf2/HO-1 signaling pathway promotes ferroptosis. Furthermore, some factors also participate in the occurrence of ferroptosis under hypoxia, such as HIF-1, NCOA4, DMT1. Meanwhile, ferroptosis is related with hypoxia-related diseases, such as MIRI, cancers, and AKI. Accordingly, ferroptosis appears to be a therapeutic target for hypoxia-related diseases.
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