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. 2022 Apr 11;13:881809. doi: 10.3389/fneur.2022.881809

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Copyright © 2022 Fang, Ding, Du, Wang and Li.

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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Crosstalk between ferroptosis and other pathological processes in stroke. As shown in the figure, the pathological stimulation caused by stroke causes ferroptosis in damaged neurons; and as one of the core events in cell injury, ferroptosis can then further promote neuroinflammation, autophagy, and apoptosis. Ferroptosis is triggered interactively with these pathological processes and participates in a close one-way or even two-way relationship so that, in the process of stroke, these key constituents initiate a variety of cascade reactions and jointly determine the survival of neurons.