Achieving Life through Death: Redox Biology of Lipid Peroxidation in Ferroptosis
Autor: | Georgy K. Vladimirov, Tamil S. Anthonymuthu, Valerian E. Kagan, Yulia Y. Tyurina, Caroline C. Philpott, Hülya Bayır, Qin Yang, Sarju J. Patel, Andrew M. Lamade, Andrew A. Amoscato |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Iron
Clinical Biochemistry Phospholipid Context (language use) Oxidative phosphorylation Biology GPX4 01 natural sciences Biochemistry Article Lipid peroxidation chemistry.chemical_compound Lipoxygenase Drug Discovery medicine Ferroptosis Humans Molecular Biology Pharmacology 010405 organic chemistry Neurodegeneration Brain RNA-Binding Proteins Lipoxygenases medicine.disease Glutathione 0104 chemical sciences Cell biology DNA-Binding Proteins chemistry Peroxidases biology.protein Molecular Medicine Lipid Peroxidation Oxidation-Reduction Intracellular |
Zdroj: | Cell Chem Biol |
Popis: | Redox balance is essential for normal brain, hence dis-coordinated oxidative reactions leading to neuronal death, including programs of regulated death, are commonly viewed as an inevitable pathogenic penalty for acute neuro-injury and neurodegenerative diseases. Ferroptosis is one of these programs triggered by dyshomeostasis of three metabolic pillars: iron, thiols, and polyunsaturated phospholipids. This review focuses on: (1) lipid peroxidation (LPO) as the major instrument of cell demise, (2) iron as its catalytic mechanism, and (3) thiols as regulators of pro-ferroptotic signals, hydroperoxy lipids. Given the central role of LPO, we discuss the engagement of selective and specific enzymatic pathways versus random free radical chemical reactions in the context of the phospholipid substrates, their biosynthesis, intracellular location, and related oxygenating machinery as participants in ferroptotic cascades. These concepts are discussed in the light of emerging neuro-therapeutic approaches controlling intracellular production of pro-ferroptotic phospholipid signals and their non-cell-autonomous spreading, leading to ferroptosis-associated necroinflammation. |
Databáze: | OpenAIRE |
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