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. 2022 Aug 5;9:966478. doi: 10.3389/fmolb.2022.966478

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Copyright © 2022 Ren, Chen, Wang and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanism of ferroptosis following ICH by inhibiting cystine/glutamate antiporter (System Xc⁻). After ICH occurs, excessive glutamate (Glu) around neurons inhibits the activity of System Xc⁻ and the transfer of cysteine (Cys), leading to reduction of glutathione (GSH) synthesis, which reduces the activity of glutathione peroxidase 4 (GPX4), resulting in excessive reactive oxygen species (ROS) and lipid peroxide levels which cannot be scavenged, thereby leading to neuronal ferroptosis, cell dysfunction, and secondary brain injury (SBI) caused by ICH.