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. 2021 Apr 6;12(4):358. doi: 10.1038/s41419-021-03640-9

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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. 4 — Damaged mitochondria lead to the release of mROS, oxidative mtDNA and mitochondria or its components-containing EVs under stress(hypoxia). (1) The oxidative mtDNA in resident cells increases inflammatory cytokines such as IL-1β and IL-18 through activating NOD (Nucleotide binding oligomerization domain)-like receptors (NLRP3) inflammasome pathway. (2) mtDNA that enter endolysome pathway through endocytosis into the receptor cells via EVs and by mitochondria-derived vesicles (MDVs) acts on Toll-like receptor 9 (TLR9)–myeloid differentiation primary response protein 88 (MYD88)–nuclear factor-kB (NF-kB) signaling for pro-inflammatory gene expression. (3) Damaged mitochondria enter into the recipient cells via EVs, which induce the generation of mROS that lead to the increased secretion of inflammatory cytokines, such as tumor necrosis factor (TNF) and Type I interferon (IFN) in recipient cells. (4) In addition, damaged mitochondria can be degraded through mitophagy, and mitochondrial miRNA and protein can be detected as diagnostic markers.