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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Nat+Chem+Biol 2017 ; 13 (1): 81-90 Nephropedia Template TP
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Oxidized Arachidonic/Adrenic Phosphatidylethanolamines Navigate Cells to Ferroptosis #MMPMID27842066
Kagan VE; Mao G; Qu F; Angeli JPF; Doll S; Croix CS; Dar HH; Liu B; Tyurin VA; Ritov VB; Kapralov AA; Amoscato AA; Jiang J; Anthonymuthu T; Mohammadyani D; Yang Q; Proneth B; Klein-Seetharaman J; Watkins S; Bahar I; Greenberger J; Mallampalli RK; Stockwell BR; Tyurina YY; Conrad M; Bay?r H
Nat Chem Biol 2017[Jan]; 13 (1): 81-90 PMID27842066show ga
Enigmatic lipid peroxidation products have been claimed as the proximate executioners of ferroptosis - a specialized death program triggered by insufficiency of glutathione peroxidase 4 (GPX4). Here, by using quantitative redox lipidomics, reverse genetics, bioinformatics and systems biology we discovered that execution of ferroptosis involves a highly organized oxygenation center, whereby only one class of phospholipids, phosphatidylethanolamines (PE), undergoes oxidation in the ER-associated compartments with the specificity towards two fatty acyls ? arachidonoyl (AA) and adrenoyl (AdA). Suppression of AA or AdA esterification into PE by genetic or pharmacological inhibition of acyl-CoA synthase 4 acts as a specific anti-ferroptotic rescue pathway. Lipoxygenases (LOX) generate doubly- and triply-oxygenated (15-hydroperoxy)-di-acylated PE species which act as death signals while tocopherols and tocotrienols suppress LOX and protect against ferroptosis suggesting an unforeseen homeostatic physiological role of vitamin E. This oxidative PE death pathway may also represent a target for drug discovery.