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Duchenne muscular dystrophy (DMD) is a monogenic muscle\u2010wasting disease that could potentially benefit from the development of CRISPR therapy. It is commonly associated with mutations that disrupt the reading frame of the <jats:italic>DMD<\/jats:italic> gene that encodes dystrophin, an essential scaffolding protein that stabilizes striated muscles and protects them from contractile\u2010induced damage. CRISPR enables the rapid generation of various animal models harboring mutations that closely simulates the wide variety of mutations observed in DMD patients. These models provide a platform for the testing of sequence\u2010specific interventions like CRISPR therapy that aim to reframe or skip DMD mutations to restore functional dystrophin expression.<\/jats:p><jats:p>This article is categorized under:<jats:list list-type=\"simple\">\n<jats:list-item><jats:p>Congenital Diseases &gt; Genetics\/Genomics\/Epigenetics<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p>","DOI":"10.1002\/wsbm.1580","type":"journal-article","created":{"date-parts":[[2022,8,1]],"date-time":"2022-08-01T02:04:05Z","timestamp":1659319445000},"source":"Crossref","is-referenced-by-count":23,"title":["<scp>CRISPR<\/scp> applications for Duchenne muscular dystrophy: From animal models to potential therapies"],"prefix":"10.1002","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7553-5163","authenticated-orcid":false,"given":"Yu C. 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