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. 2021 Oct 1;9(10):1366. doi: 10.3390/biomedicines9101366

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Schematic of the immunological events following muscle damage in Duchenne muscular dystrophy (DMD). An inflammatory response is activated in dystrophic muscle cells, and immune cells, including neutrophils and macrophages, are recruited to the sites of damage. The expression of inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO), hypochlorous acid (HOCl), and pro-inflammatory cytokines, including interleukin (IL) 6 (IL-6), tumor necrosis factor alpha (TNF-α) and IL-1β, followed by anti-inflammatory cytokines, including IL-10, IL-4 and transforming growth factor beta (TGF-β), combined with the release of DAMPs including single stranded RNA (ssRNA) and high mobility group box protein 1 (HMGB1), initially results in regeneration of the muscle. However, continuous release of cytokines and DAMPs results in prolonged inflammation. This chronic inflammatory condition leads to impaired muscle repair followed by necrosis of muscle cells and accumulation of excessive fatty connective tissue leading to fibrosis.