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. 2021 Jun 5;12:323. doi: 10.1186/s13287-021-02389-4

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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. 1 — Functions and mechanisms of stem cells and exosomes in necrotizing enterocolitis (NEC). Stem cells and exosomes exert beneficial effects to NEC via various signaling pathways. Mesenchymal stem cells (MSCs) secrete cytokines and growth factors including interleukin (IL)-6, vascular endothelial growth factor (VEGF), and hepatocyte growth factor (HGF). Downregulation of prolyl hydroxylase 2 (PHD2) activates the nuclear factor-κB (NF-κB) signaling in MSCs, which increases the paracrine release of insulin-like growth factor (IGF)-1 and transforming growth factor-beta 2 (TGF-β2). MSCs increase the expression of cyclooxygenase 2 (COX-2) in stromal cells by the paracrine manner. Exosome (Exs) contains non-coding RNAs (ncRNAs) beneficial to NEC injury. Milk-derived Exs increase goblet cell expression markers trefoil factor 3 (TFF3) and mucin 2 (MUC2), as well as the expression of endoplasmic reticulum chaperone protein glucose-regulated protein 94 (GRP94). Both MSCs and MSC-derived Exs can activate the Wnt/β-catenin signaling pathway, which increases ISC viability and intestinal regeneration