Ferroptosis Regulation by Nutrient Signalling

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 co...

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Bibliographic Details
Published in:Nutrition research reviews 2022-12, Vol.35 (2), p.282-294
Main Authors: Qi, Yingao, Zhang, Xiaoli, Wu, Zhihui, Tian, Min, Chen, Fang, Guan, Wutai, Zhang, Shihai
Format: Article
Language:English
Subjects:
Amino acids
AMP-activated protein kinase
Apoptosis
Cell death
Cell membranes
Coenzyme Q10
Cytochrome
Diet
Dietary intake
Enzymes
Exports
Fatty acid composition
Fatty acids
Ferroptosis
Food intake
Hemoglobin
Homeostasis
Iron
Kinases
Lipid peroxidation
Lipids
Lipoproteins
Molecular interactions
Nutrients
Oxidation
Peroxidation
Phospholipids
Polyunsaturated fatty acids
Proteins
Rapamycin
Selenium
Signal transduction
Small intestine
TOR protein
Tuberous sclerosis
Vitamin E
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Summary: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 Q10) 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.
ISSN:0954-4224
1475-2700
DOI:10.1017/S0954422421000226