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. 2023 Jan 16;21:14. doi: 10.1186/s12951-023-01778-6

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© The Author(s) 2023

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. 4 — Mechanisms of exosomes on TBI injuries. a Exosomes could attenuate early inflammatory response via reducing inflammatory, polarizing macrophage from a pro-inflammatory M1 phenotype to a pro-regenerative M2 phenotype, and reducing inflammatory cytokines release. b Exosomes could enhance cell proliferation and reduce apoptosis. c Exosomes rich in miR-6924-5p could directly inhibit osteoclast formation by binding to the 3′-untranslated regions (3′ UTRs) of OCSTAMP and CXCL12. d Exosome-delivered BMP-2 promotes cartilage differentiation via Smad/RUNX2 signaling pathway. Activation of BMP-2/Smad signaling induces Runx2 expression through the activation of Smad4 and Smad5, after which Runx2 induces the expression of cartilage differentiation-related proteins, Aggrecan, Collagen II, SOX-9, and TIMP-1. e Exosomes promote angiogenesis by activating the VEGF and Hippo signaling pathways. When VEGF binds to the vascular endothelial growth factor receptor (VEGFR), the VEGF‐VEGFR interaction inhibits LATS1/2 and YAP1 phosphorylation by activating the PI3K and MAPK signaling pathways. The leads to increased expression of YAP1 in the nucleus inducing angiogenesis. f Exosomes could reduce fatty infiltration