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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. 3 — a ATP levels, b Intracellular ROS levels, c Mitochondrial membrane potential (MMP) levels, and d Cell viability of bleomycin-treated TC-1 cells (BLM-TC-1) after treatment with different engineered hMSCs (n = 3, biologically independent cells for each). Impacts of Pg treatment on e ATP levels, f Intracellular ROS levels, g MMP levels, and h Cell viability of BLM-TC-1 cells (n = 3, biologically independent cells for each). Impacts of PGC-1α expression on i ATP levels, j Intracellular ROS levels, k MMP levels, and l Cell viability of BLM-TC-1 cells (n = 3, biologically independent cells for each). m Illustration showing the possible therapeutic mechanism of treating hMSC with Pg for augmented mitochondrial transfer via promoting the PGC-1α-dependent mitochondrial biogenesis. Data are presented as means ± SD. Statistical significance was analyzed using ordinary one-way ANOVA.