脂质代谢
脂质过氧化
GPX4
程序性细胞死亡
细胞生物学
细胞
细胞损伤
生物
癌细胞
新陈代谢
化学
生物化学
氧化应激
细胞凋亡
癌症
超氧化物歧化酶
遗传学
谷胱甘肽过氧化物酶
作者
Zhi Lin,Jiao Liu,Rui Kang,Minghua Yang,Daolin Tang
标识
DOI:10.1002/adbi.202100396
摘要
Abstract Lipid metabolism is a complex biochemical process that participates in the regulation of cell survival and death. Ferroptosis is a form of iron‐dependent regulated cell death driven by abnormal lipid metabolism, leading to lipid peroxidation and subsequent plasma membrane rupture. A variety of antioxidant systems and membrane repair pathways can diminish oxidative damage, enabling survival and growth in response to ferroptotic signals. Such impairment of ferroptosis machinery is implicated in various pathological conditions and diseases, especially cancer and tissue damage. It is discussed here how lipid metabolism pathways, including lipid synthesis, degradation, storage, transformation, and utilization, modulate ferroptosis sensitivity or tolerance in different models, especially cancer.
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