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. 2024 Feb 23;43(7):1164–1186. doi: 10.1038/s44318-024-00055-y

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV5 — (1) Ferroptosis inducers promote the formation of lipid peroxides at the plasma membrane which cause and increase in membrane tension. (2) Mechanosensitive ion channels (Piezo-1 and TRP channels) open is response to increased membrane tension, resulting in the entry of calcium and sodium ions and the release of potassium ions. These non-selective ion fluxes cause an increase in the cell volume and swelling (3) Following this step, NINJ1 is activated, possibly because of ion disbalance, swelling or a yet unrecognized signal, and oligomerizes to form amphipathic filaments. Initially these filaments cause only small lesions that allow the entry and exit of small molecules, such as DNA-binding dyes. (4) Eventually NINJ1 lesions cause complete membrane rupture and cell lysis. As a consequence of NINJ1-dependent PMR, ferroptotic cells start to leak intracellular content among them many DAMPs that can drive inflammation.