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. 2021 Apr 21;44(5):1815–1830. doi: 10.1007/s10753-021-01460-9

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© The Author(s) 2021

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/.

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Fig. 6 — Exosomal miR-671 targets TGFBR2 and reduces Smad2 phosphorylation. a Protein levels of TGFBR2, Smad2 and the phosphorylation of Smad2 in each group of cardiomyocytes examined by western blot analysis; b Viability of cardiomyocytes after si-TGFBR2 transfection measured by the MTT assay; c Apoptosis of cardiomyocytes after si-TGFBR2 transfection examined by flow cytometry; d Protein levels of apoptosis-related factors (Bax and Bcl-2) and the fibrosis-related factor α-SMA in cardiomyocytes after si-TGFBR2 transfection determined by western blot analysis; e Production of pro-inflammatory cytokines (IL-6 and TNF-α) in cardiomyocytes after si-TGFBR2 transfection determined using ELISA kits. Data were collected from three experiments and exhibited as mean ± SEM. Differences were analyzed by unpaired t test (b, c) or two-way ANOVA (a, d, and e); *p < 0.05 vs. Control group; #p < 0.05 vs. OGD group; &p < 0.05 vs. Exo-NC group; @p <0.05 vs. Exo-inhibitor + si-NC group.