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. 2019 Jun 27;10:196. doi: 10.1186/s13287-019-1289-7

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 2 — Paracrine effects of the ASC secretome and involved pathways. ASCs secrete IGF-1, SOD-3, miRNA-301a, and exosomes for improving the effect of anti-apoptosis or pro-survival through regulating cell cycle, N-Cadherin/ERK/Nrf2, ASK-1 and NFγB/p38/JNK, Wnt/β-Catenin, cyclin D1, Bcl-2 and Bax, respectively. ASC-derived microvesicles perform the pro-angiogenesis effect via delivery of miRNA-126 and miRNA-31 through ERK1/2/MAPK and FIH-1 pathways, respectively. The conditioned medium of ASCs exerts the anti-inflammation effect through IFN-γ/IDO and PGE₂/EP2/4 signaling pathways, which also can recruit circulating EPCs through CXCL12/SDF-1α pathway. The anti-cardiac remodeling effect is mediated by exosomes through MAPK/PI3K pathway and HGF released from ASCs