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. 2022 Nov 8;13:1020918. doi: 10.3389/fphar.2022.1020918

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Copyright © 2022 Wei, Xie, Wei, Zhao, Ren, Feng and Xu.

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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Possible molecular mechanisms of ferroptosis and potential therapeutic targets in ischemic stroke. The decrease of GSH, GPX4, tau protein, and the increase of lipoxygenase (LOX), and BBB permeability, can lead to the occurrence of ferroptosis in ischemic stroke. Iron chelators like deferoxamine (DFO), ciclopirox (CPX) and 2,2-bipyridyl (2,2-BP) can inhibit ferroptosis; Lipoxygenase inhibitors like Baicalein, Vitamin E, ML351 and Zileuton can suppress LOXs activity to rescue cells from ferroptosis; Ferrostatin-1 (Fer-1) and Liproxstatin-1 (Lip-1) inhibit radical-trapping antioxidants which activate LOXs to prevent ferroptosis in cells.