{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T12:28:44Z","timestamp":1790512124531,"version":"4.1.0"},"reference-count":76,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,10,24]],"date-time":"2020-10-24T00:00:00Z","timestamp":1603497600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R21NS106313"],"award-info":[{"award-number":["R21NS106313"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R56AG051501"],"award-info":[{"award-number":["R56AG051501"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Impairment of muscle biogenesis contributes to the progression of Duchenne muscular dystrophy (DMD).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>As a muscle enriched microRNA that has been implicated in muscle biogenesis, the role of miR\u2010133b in DMD remains unknown.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            To assess miR\u2010133b function in DMD\u2010affected skeletal muscles, we genetically ablated miR\u2010133b in the\n                            <jats:italic>mdx<\/jats:italic>\n                            mouse model of DMD.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We show that deletion of miR\u2010133b exacerbates the dystrophic phenotype of DMD\u2010afflicted skeletal muscle by dysregulating muscle stem cells involved in muscle biogenesis, in addition to affecting signalling pathways related to inflammation and fibrosis.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Our results provide evidence that miR\u2010133b may underlie DMD pathology by affecting the proliferation and differentiation of muscle stem cells.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Duchenne muscular dystrophy (DMD) is characterized by progressive skeletal muscle degeneration. No treatments are currently available to prevent the disease. While the muscle enriched microRNA miR\u2010133b has been implicated in muscle biogenesis, its role in DMD remains unknown. To assess miR\u2010133b function in DMD\u2010affected skeletal muscles, we genetically ablated miR\u2010133b in the\n                      <jats:italic>mdx<\/jats:italic>\n                      mouse model of DMD. In the absence of miR\u2010133b, the tibialis anterior muscle of P30\n                      <jats:italic>mdx<\/jats:italic>\n                      mice is smaller in size and exhibits a thickened interstitial space containing more mononucleated cells. Additional analysis revealed that miR\u2010133b deletion influences muscle fibre regeneration, satellite cell proliferation and differentiation, and induces widespread transcriptomic changes in\n                      <jats:italic>mdx<\/jats:italic>\n                      muscle. These include known miR\u2010133b targets as well as genes involved in cell proliferation and fibrosis. Altogether, our data demonstrate that skeletal muscles utilize miR\u2010133b to mitigate the deleterious effects of DMD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp280405","type":"journal-article","created":{"date-parts":[[2020,9,29]],"date-time":"2020-09-29T18:24:04Z","timestamp":1601403844000},"page":"171-192","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["The microRNA miR\u2010133b functions to slow Duchenne muscular dystrophy pathogenesis"],"prefix":"10.1113","volume":"599","author":[{"given":"Thomas","family":"Taetzsch","sequence":"first","affiliation":[{"name":"Department of Molecular Biology Cell Biology and Biochemistry Brown University  Providence RI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dillon","family":"Shapiro","sequence":"additional","affiliation":[{"name":"Molecular Biology Cell Biology, &amp; Biochemistry Graduate Program Brown University  Providence RI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Randa","family":"Eldosougi","sequence":"additional","affiliation":[{"name":"Fralin Biomedical Research Institute at Virginia Tech Carilion  Roanoke VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0052-6294","authenticated-orcid":false,"given":"Tracey","family":"Myers","sequence":"additional","affiliation":[{"name":"Fralin Biomedical Research Institute at Virginia Tech Carilion  Roanoke VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1354-7609","authenticated-orcid":false,"given":"Robert E.","family":"Settlage","sequence":"additional","affiliation":[{"name":"Advanced Research Computing Virginia Tech  Blacksburg VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0375-4532","authenticated-orcid":false,"given":"Gregorio","family":"Valdez","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology Cell Biology and Biochemistry Brown University  Providence RI USA"},{"name":"Center for Translational Neuroscience Robert J. and Nancy D. 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