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. 2021 Aug 3;12:433. doi: 10.1186/s13287-021-02511-6

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© The Author(s) 2021

Open AccessThis 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. 1 — Identification of MenSC-derived small EVs and their therapeutic potentials for tissue repair in various diseases. Small EVs from MenSCs consist of regulatory proteins, RNAs, and DNAs, lipids, and siginaling peptides promoting regenerative repair of wounded cells and tissues. MenSC-derived small EVs are positive for the expression of CD9, CD63, CD81, HSP70, HSP90, and TSG101, and they are negative for Rab5 and calnexin. The expression of HSP60 and Alix, which are positive for universal MSC-derived small EVs, need to be recognized for further verification. The therapeutic potential of MenSC-derived small EVs in various diseases, including fulminant hepatic failure (FHF; via inhibition of hepatocyte apoptosis by bioactive molecules), myocardial infarction (MI, via secreted microRNA-21), pulmonary fibrosis (via secreted microRNA-lethal-7), prostate cancer (PC; via suppression of angiogenesis by ROS signaling), cutaneous wound (via increase in VEGF-A and activation of NF-κB pathway), type-1 diabetes mellitus (T1DM; via generation of β islets to secrete insulin by Pdx-1 signaling), aged fertility (via regulation of ROS signaling and increase in pluripotent activity), and some potential diseases (such as inflammatory and neurodegenerative diseases)