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. 2018 Nov 8;8:16519. doi: 10.1038/s41598-018-34879-6

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© The Author(s) 2018

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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Exosomes protect against mitochondrial triggers of apoptosis in Dys-iCMs. (a) Dys1-iCM mitochondria displayed higher levels of Bax (green) positive mitochondria (Mitotracker, red) following stress which was ameliorated following exosome exposure. Exosome exposure also (b,c) prevented stress-induced loss of mitochondrial membrane potential; (d,e) delayed mPTP formation, (f) decreased % caspase positive cells; and (g,h) mitigated stress-induced increases in PI positive nuclei. n = 3/group. *p < 0.05 vehicle stress vs. vehicle no stress, ^#p < 0.05 exosome exposure vs. vehicle stress.