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. 2020 Dec 24;45:101157. doi: 10.1016/j.molmet.2020.101157

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© 2020 The Author(s)

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Loss of utrophin in dystrophin-deficient muscles impairs adaptive remodeling and protection from contraction-induced injury after low-frequency stimulation (LFS). (A) Representative tibialis anterior (TA) muscle fibrosis staining (left) and quantification (right) (n = 6–8/group). Scale bar = 50 μm. (B–D) Relative tetanic force production (% of maximal) of TA muscles (in situ) at various stimulation frequencies in BL/10 (B), mdx (C), and dko (D) mice (n = 6–16/group). (E and F) Eccentric contraction-induced injury in TA muscles (in situ) of mdx (E) and dko (F) mice (n = 6–16/group). (G) Degree of protection during TA eccentric contraction-induced injury (n = 6–7/group). (H) Summary describing the role of dystrophin and utrophin in metabolic and contractile remodeling with LFS. Created with BioRender.com. Data are means ± SEM; two-way ANOVA followed by Tukey's multiple comparison test (A); † difference to BL/10; ‡ difference to mdx; unpaired Student's t-test (B–G); ∗p < 0.05, ∗∗p < 0.01.