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. 2022 Jan 3;20:1. doi: 10.1186/s12964-021-00806-y

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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. 2 — VEGF: vascular endothelial growth factor, MMPs: matrix metalloproteinases, UPA: urokinase-type plasminogen activator, HUVECS:Human umbilical vein endothelial cells. Mechanisms by which sEVs promote angiogenesis when secreted to distant organs. When sEVs reach distant organs, TSPAN8 and other four asppanins carried on them can enhance the expression of pro-vascular factors such as VEGF, MMPs and UPA. Secondly, miRNA, circ-iars and other components carried by pancreatic cancer-derived sEVs promote angiogenesis by inducing HMVEC growth. In addition, non-tumor cell-derived sEVs can also promote angiogenesis. TAMS-derived sEVs promote angiogenesis by activating the TGF-β signaling pathway and down-regulating TGFbR3