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. 2022 Nov 29;30(2):304–312. doi: 10.1038/s41418-022-01094-w

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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. 1 — Mitochondria contain DAMPs that can be exposed upon mitochondrial stress and damage. These DAMPs include succinate, N-formyl peptides, dsRNA, mtDNA, ROS, cardiolipin, and ATP. Loss or exposure of these DAMPs activates several immune pathways including transcription of type I interferons and NF-κB target genes, inflammasome activation, and the recruitment of immune cells.