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. 2022 May 5;38(10):1229–1247. doi: 10.1007/s12264-022-00859-0

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© The Author(s) 2022

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Fig. 3 — Ferroptosis during cerebral ischemia. Normally, GPX4 uses GSH to catalyze lipid hydroperoxides into alcohols. Increased extracellular glutamate inhibits the activity of System Xc⁻ as well as the cysteine-GSH-GPX4 axis. Meanwhile, Ca²⁺ overload activates cPLA2α to provide substrates for lipid peroxidation. Fe²⁺-activated lipoxygenase (LOX) also participates in this process. Increased redox-active iron and overwhelming lipid peroxidation contribute to ferroptosis. cPLA2α, cytosolic phospholipase A2α; GPX4, γ‐L‐glutamyl‐L‐cysteinylglycine peroxidase 4; GSH, glutathione; GSSG, oxidized glutathione; LOX, lipoxygenase; PUFA, polyunsaturated fatty acid; TRF, transferrin.