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. 2022 Feb 3;16:799753. doi: 10.3389/fncel.2022.799753

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Copyright © 2022 Zhang, Khan, Liu, Zhang, Li, Wu, Tang, Xue and Yong.

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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Overview of ferroptosis pathways following ICH. Dysfunction of the cystine/glutamate antiporter after ICH leads to decreased synthesis of glutathione (GSH) and activity of glutathione peroxidase 4 (GPX4). Iron released from lysed erythrocytes can produce highly toxic hydroxyl radicals to attack DNA, proteins, and lipid membranes. The deficiency of GPX4 combined with the presence of toxic iron leads to the accumulation of lipid peroxides and the execution of ferroptosis. ROS, reactive oxygen species.