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. 2021 Aug 10;12(8):782. doi: 10.1038/s41419-021-04054-3

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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. 2 — The accumulation of lipid peroxides in endothelial cells that cause ferroptosis derived from two pathways. The extracellular ox-LDL causes endothelial cell mitochondrial damage, and intracellular iron overload causes lipid peroxide accumulation, which can be reserved by fer-1. Meanwhile, ATF3 inhibits its clearance pathway, and has a protective effect on atherosclerosis by reducing the damage of elastic membrane by inhibiting the PI3K-MMP3 pathway. The ferroptosis of endothelial cell and elastic lamina damage leads to endothelial dysfunction promoting the formation of AS.