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. 2023 Sep 18;14:5781. doi: 10.1038/s41467-023-41529-7

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© The Author(s) 2023

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. 6 — a Relative human mtDNA in mice lungs after treatment with indicated engineered hMSC (n = 3 biologically independent animals). b Heatmap of significantly differentially expressed mitochondria-related genes after the indicated treatments (n = 3 biologically independent animals). c Enriched GO pathways based on the significant differentially expressed genes between Fe-hMSC and Pg-Fe-hMSC. d String analysis identified genes in PF mice treated with Pg-Fe-hMSC that were associated with mitochondrial functions. PCR analyses of differentially expressed mitochondria-related genes of e MT-CO1, f MT-CO2, g MT-ND1, h MT-ND3, i TOMM5, and j TOMM6 after the indicated treatments (n = 3 biologically independent animals for each). Data are presented as means ± SD. Statistical significance was analyzed using ordinary one-way ANOVA.