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. 2021 Apr 7;78(11):4867–4891. doi: 10.1007/s00018-021-03821-x

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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/.

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Fig. 7 — Altered functioning of DMD satellite cells. Pathological alterations related to satellite cell function are listed in boxes. Examples of disturbed signaling pathways, altered gene expression and epigenetic changes are shown in the boxes. Molecular mechanisms underlying pathologies in DMD satellite cells are described in the text. Abbreviations: myogenic factor 5 (Myf5), microtubule affinity regulating kinase 2 (MARK2), partitioning defective protein 3 (PARD3), phosphorylated Aurora kinase (pAURK), reactive oxygen species (ROS), fibroblast growth factor 2 (FGF2), heme oxygenase 1 (HO-1), myoblast determination protein (MYOD), myogenin (MYOG)