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. 2021 Mar 17;12(4):289. doi: 10.1038/s41419-021-03559-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — p53 plays a dual role in the regulation of ferroptosis through transcriptional or posttranslational mechanisms in different contexts. On one hand, p53 induces ferroptosis through inhibition of SLC7A11 or upregulation of GSL2 and SAT1–ALOX pathway. On the other hand, p53 also inhibits ferroptosis through inhibition of DPP4 activity or by the transcriptional activation of CDKN1A/p21. ALOX arachidonate lipoxygenase, CDKN1A cyclin-dependent kinase inhibitor 1 A, DPP4 dipeptidyl-peptidase-4, GLS2 glutaminase 2, GSH glutathione, NOX1 NADPH oxidase 1, ROS reactive oxygen species, SAT1 spermidine/spermine N1-acetyltransferase 1, SLC7A11 solute carrier family 7 member 11.