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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. 3 — Chronic inflammation in DMD skeletal muscles. Pathological alterations related to chronic inflammation are listed in boxes. Arrows illustrate the release of various factors, while dashed line arrows depict the transformation of one type of cell to another. Molecular mechanisms underlying ongoing processes of sarcolemma instability and DAMP release a, activation of the innate immune response b, development of adaptive immune response c, muscle fibrosis d, and inter- and intracellular signaling driving inflammatory response e are described in the text. Abbreviations: extracellular matrix (ECM), damage-associated molecular patterns (DAMPs), major histocompatibility complex I (MHCI), matrix metalloproteases (MMP), fibroadipogenic progenitors (FAPs), interferon γ (INFγ), tissue necrosis factor (TNF), receptor of TNF (TNFR), TNFR Associated Factor 2 (TRAF2), IκB kinase (IKK), IKB, phosphorylated IKB (P-IKB), nuclear factor-κB (NF-κB), high-mobility group box 1 (HMGB1), Toll-like receptors (TLR2/4), TNFR associated factor 6 (TRAF6), myeloid differentiation primary response 88 (MYD88), interleukin (IL), transforming growth factor-β (TGFβ)