线粒体
GPX4
细胞生物学
程序性细胞死亡
活性氧
生物
氧化磷酸化
癌细胞
信号转导
功能(生物学)
细胞凋亡
癌症
氧化应激
生物化学
遗传学
过氧化氢酶
谷胱甘肽过氧化物酶
作者
Kai Sun,Yuan Zhi,Wenhao Ren,Shaoming Li,Xiaoqing Zhou,Ling Gao,Keqian Zhi
标识
DOI:10.1016/j.biopha.2023.115892
摘要
Ferroptosis is an iron-dependent regulated cell death, mainly manifested by the production of reactive oxygen species and accumulation of lipid peroxides. It is distinct from other forms of cell death with regard to morphology and biochemistry, particularly in disrupting mitochondrial function. Mitochondria are essential compartments where the organism generates energy and are closely associated with the fate of ferroptosis. Currently, researchers focus on the potential value of ferroptosis and mitochondria for overcoming drug sensitivity and assisting in cancer therapy. In this review, we summarize the main mechanisms of ferroptosis (the GPX4-realated pathway, FSP1-related pathway, and iron metabolism pathway) and the functions and regulating pathways of mitochondria (the TCA cycle, oxidative phosphorylation, mitochondrial regulation of iron ions, and mtDNA) in ferroptosis. We believe that exploring the role of mitochondria in ferroptosis will help us understand the potential regulatory mechanisms of ferroptosis in cancer and help us find new therapeutic targets.
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