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. 2024 Mar 19;31:30. doi: 10.1186/s12929-024-01019-4

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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. 6 — Efficient encapsulation of let-7a-5p in MSCs-derived EVs via the CNP platform for acute lung injury treatment. Our results from the CNP platform, cell model, and rat model strongly confirm the following mechanism: The CNP platform provides an efficient method for producing engineered miRNA-enriched EVs with high specificity. These EV-let-7a-5p effectively attenuate Smad2/3 activation induced by TGF-β. Additionally, our observations indicate that EV-let-7a-5p regulate the induction of M2 macrophages in response to a fibrotic microenvironment resulting from pulmonary injury. Hence, EV-let-7a-5p hold promise for improving adverse lung conditions associated with ALI. The illustration was created with BioRender.com