mTORC1型
安普克
激酶
多不饱和脂肪酸
蛋白激酶A
细胞生物学
生物
GPX4
脂质过氧化
化学
氧化应激
程序性细胞死亡
信号转导
生物化学
脂肪酸
PI3K/AKT/mTOR通路
细胞凋亡
谷胱甘肽过氧化物酶
过氧化氢酶
作者
Yingao Qi,Xiaoli Zhang,Zhihui Wu,Min Tian,Fang Chen,Wutai Guan,Shihai Zhang
出处
期刊:Nutrition Research Reviews
[Cambridge University Press]
日期:2021-07-08
卷期号:35 (2): 282-294
被引量:23
标识
DOI:10.1017/s0954422421000226
摘要
Abstract Tremendous progress has been made in the field of ferroptosis since this regulated cell death process was first named in 2012. Ferroptosis is initiated upon redox imbalance and driven by excessive phospholipid peroxidation. Levels of multiple intracellular nutrients (iron, selenium, vitamin E and coenzyme Q 10 ) are intimately related to the cellular antioxidant system and participate in the regulation of ferroptosis. Dietary intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) regulates ferroptosis by directly modifying the fatty acid composition in cell membranes. In addition, amino acids and glucose (energy stress) manipulate the ferroptosis pathway through the nutrient-sensitive kinases mechanistic target of rapamycin complex 1 (mTORC1) and AMP-activated protein kinase (AMPK). Understanding the molecular interaction between nutrient signals and ferroptosis sensors might help in the identification of the roles of ferroptosis in normal physiology and in the development of novel pharmacological targets for the treatment of ferroptosis-related diseases.
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