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. 2021 Jun 28;7:149. doi: 10.1038/s41420-021-00553-6

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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 — Intracellular mechanism of ferroptosis regulated at various levels. In mitochondria, glutaminolysis increase ROS production via unkown mechanism and contributes to ferroptosis. At nuclear level, histone modifications such as ubiquitination, demethylation, or deacetylation; DNA transcriptional regulation via hypomethylation at specific loci, transcriptional factors, lncRNA; and metabolic regulation through proteins; inhibit ferroptosis.