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

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© The Author(s) 2022

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 — MOMP activates several pro-inflammatory pathways. (1) Under caspase-inhibited conditions MOMP causes IAP degradation which subsequently leads to NIK stabilisation and accumulation followed by the transcription of NF-κB target genes. In addition, degradation of IAPs activates caspase-1 and caspase-8 leading to processing and release of IL-1β and IL-18. (2) Cytosolic release of mtDNA leads to recognition of cGAS which subsequently forms cGAMP out of GTP and ATP. cGAMP is a second messenger for ER-resident STING initiating its activating and the subsequent transcription of NF-κB target genes and type I interferons. (3) Release of cytosolic dsRNA leads to its recognition by RIG-I and MDA5, followed by activation of mitochondria-localised MAVS and a type I interferon response.