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We have previously shown that disruption of\n                    <jats:italic>Mss51<\/jats:italic>\n                    , a mammalian skeletal muscle protein that localizes to the mitochondria, results in enhanced muscle oxygen consumption rate, increased endurance capacity, and improved limb muscle strength in mice with wildtype background. Here, we investigate whether\n                    <jats:italic>Mss51<\/jats:italic>\n                    deletion in the\n                    <jats:italic>mdx<\/jats:italic>\n                    murine model of Duchenne muscular dystrophy (\n                    <jats:italic>mdx\u2010Mss51<\/jats:italic>\n                    KO) counteracts the muscle pathology and mitochondrial irregularities observed in\n                    <jats:italic>mdx<\/jats:italic>\n                    mice. We found that\n                    <jats:italic>mdx\u2010Mss51<\/jats:italic>\n                    KO mice had increased myofiber oxygen consumption rates and an amelioration of muscle histopathology compared to\n                    <jats:italic>mdx<\/jats:italic>\n                    counterparts. This corresponded with greater treadmill endurance and less percent fatigue in muscle physiology, but no improvement in forelimb grip strength or limb muscle force production. These findings suggest that although\n                    <jats:italic>Mss51<\/jats:italic>\n                    deletion ameliorates the skeletal muscle mitochondrial respiration defects in\n                    <jats:italic>mdx<\/jats:italic>\n                    and improves fatigue resistance in vivo, the lack of improvement in force production suggests that this target alone may be insufficient for a therapeutic effect.\n                  <\/jats:p>","DOI":"10.1096\/fj.202002106rr","type":"journal-article","created":{"date-parts":[[2021,1,14]],"date-time":"2021-01-14T22:14:15Z","timestamp":1610662455000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["<i>Mss51<\/i>\n                    deletion increases endurance and ameliorates histopathology in the\n                    <i>mdx<\/i>\n                    mouse model of Duchenne muscular dystrophy"],"prefix":"10.1096","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5323-536X","authenticated-orcid":false,"given":"Yazmin I.","family":"Rovira Gonzalez","sequence":"first","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"},{"name":"Cellular and Molecular Medicine Graduate Program Johns Hopkins School of Medicine Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adam L.","family":"Moyer","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"},{"name":"Cellular and Molecular Medicine Graduate Program Johns Hopkins School of Medicine Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicolas J.","family":"LeTexier","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"August D.","family":"Bratti","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Siyuan","family":"Feng","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vanessa","family":"Pe\u00f1a","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Congshan","family":"Sun","sequence":"additional","affiliation":[{"name":"The Hugo W. Moser Research Institute Kennedy Krieger Institute Baltimore MD USA"},{"name":"Departments of Neurology and Neuroscience Johns Hopkins School of Medicine Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hannah","family":"Pulcastro","sequence":"additional","affiliation":[{"name":"The Hugo W. 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