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. 2022 Jul 6;20:307. doi: 10.1186/s12967-022-03502-8

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© The Author(s) 2022

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. 6 — In vivo analysis of macrophage EVs miR-32 promotes aorta calcification by inhibited autophagy. Analysis of VSMC autophagy and osteogenic differentiation in the aorta of miR-32^−/− T2D mice after treated with macrophage EVs. A Blood glucose analysis. B IPITT analysis. C HOMA-IR analysis. D Immunohistochemisty analyzed miR-32 expression in aorta of miR-32^−/− mice, and WT mice, and miR-32^−/− injection EVs. C qRT-PCR analyzed aorta osteogenic differentiation. F, G alizarin red staining analyzed aorta calcification after macrophage EVs injection (F), and statistical analysis (G). H–K Immunofluorescence analyzed p62 and LC3 expressions in aorta (H), and statistical analyzed the puncta of p62 (I), LC3 (J), and p62-LC3 (K). 3 per 5 mice in different groups were used in the detection. *p < 0.05 and **p < 0.01. Data was shown as means ± s.e.m