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While the cause of DMD is an X-linked loss of function mutation in the gene encoding dystrophin, the exact mechanisms that perpetuate the disease progression are unknown. Our laboratory has demonstrated that pannexin 1 (Panx1 in rodents; PANX1 in humans) is critical for the development, strength, and regeneration of male skeletal muscle. In normal skeletal muscle, Panx1 is part of a multiprotein complex with dystrophin. We and others have previously shown that Panx1 levels and channel activity are dysregulated in various mouse models of DMD.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We utilized myoblast cell lines derived from DMD patients to assess PANX1 expression and function. To investigate how Panx1 dysregulation contributes to DMD, we generated a dystrophic (<jats:italic>mdx<\/jats:italic>) mouse model that lacks Panx1 (<jats:italic>Panx1<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>\/mdx<\/jats:italic>). In depth characterization of this model included histological analysis, as well as locomotor, and physiological tests such as muscle force and grip strength assessments.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Here, we demonstrate that PANX1 levels and channel function are reduced in patient-derived DMD myoblast cell lines. <jats:italic>Panx1<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>\/mdx<\/jats:italic> mice have a significantly reduced lifespan, and decreased body weight due to lean mass loss. Their <jats:italic>tibialis anterior<\/jats:italic> were more affected than their <jats:italic>soleus<\/jats:italic> muscles and displayed reduced mass, myofiber loss, increased centrally nucleated myofibers, and a lower number of muscle stem cells compared to that of <jats:italic>Panx1<\/jats:italic><jats:sup>+<jats:italic>\/<\/jats:italic>+<\/jats:sup><jats:italic>\/mdx<\/jats:italic> mice. These detrimental effects were associated with muscle and locomotor functional impairments. In vitro, PANX1 overexpression in patient-derived DMD myoblasts improved their differentiation and fusion.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Collectively, our findings suggest that PANX1\/Panx1 dysregulation in DMD exacerbates several aspects of the disease. Moreover, our results suggest a potential therapeutic benefit to increasing PANX1 levels in dystrophic muscles.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13395-024-00340-8","type":"journal-article","created":{"date-parts":[[2024,4,26]],"date-time":"2024-04-26T10:02:51Z","timestamp":1714125771000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Pannexin 1 dysregulation in Duchenne muscular dystrophy and its exacerbation of dystrophic features in mdx mice"],"prefix":"10.1186","volume":"14","author":[{"given":"Emily","family":"Freeman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"St\u00e9phanie","family":"Langlois","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcos F.","family":"Leyba","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tarek","family":"Ammar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zacharie","family":"L\u00e9ger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hugh J.","family":"McMillan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Marc","family":"Renaud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard J.","family":"Jasmin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyle N.","family":"Cowan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,4,26]]},"reference":[{"issue":"1","key":"340_CR1","doi-asserted-by":"publisher","first-page":"13903","DOI":"10.1038\/s41598-019-50444-1","volume":"9","author":"A Aguilar-Perez","year":"2019","unstructured":"Aguilar-Perez A, Pacheco-Costa R, Atkinson EG, Deosthale P, Davis HM, Essex AL, Dilley JE, Gomez L, Rupert JE, Zimmers TA, Thompson RJ, Allen MR, Plotkin LI. 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