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. 2024 Feb 12;22:60. doi: 10.1186/s12951-024-02304-y

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Activation of angiogenesis related pathways in skeletal muscles after MSC-EV treatment in vivo. Quantification of NO A and O₂⁻ B production in skeletal muscles by EPR. C (Left) Representative Western immunoblotting analysis of protein levels of eNOS, VEGF, Akt and their phosphorylated variants, caveolin and β-actin proteins in muscle tissues from ischemic (I) and non-ischemic (N) limb. (Right/Bottom) Quantitative analysis of expression and phosphorylation of eNOS, VEGF, Akt and caveolin-1. Values are presented as a ratio of ischemic (I) to non-ischemic (N) signal amplitude/protein expression and calculated as a percent (%) of signal in control tissues form vehicle (PBS)-treated animals. Mann–Whitney test, comparison to vehicle-treated samples (*P < 0.05)