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. 2020 Feb 3;11(2):88. doi: 10.1038/s41419-020-2298-2

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© The Author(s) 2020

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. 2 — The figure shows the regulatory pathways of ferroptosis, which can be roughly divided into three categories. The first one is regulated by GSH/GPX4 pathway, such as inhibition of system Xc-, sulfur transfer pathway, MVA pathway, glutamine pathway, and p53 regulatory axis. Second, the regulation mechanism of iron metabolism, such as the regulation of ATG5-ATG7-NCOA4 pathway and IREB2 related to ferritin metabolism, and the regulatory pathways of p62-Keap1-NRF2 and HSPB1 all have effects on iron. The third category is related pathways around lipid metabolism, such as P53-SAT1-ALOX15, ACSL4, LPCAT3, etc., which have effects on lipid regulation and ferroptosis. In addition, Erastin acts on mitochondria to induce ferroptosis. Also, recent studies have shown that the FSP1-CoQ10- NAD(P)H pathway exists as an independent parallel system that works cooperatively with GPX4 and glutathione to inhibit phospholipid peroxidation and ferroptosis.