{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T15:08:50Z","timestamp":1784646530008,"version":"3.55.0"},"reference-count":73,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,2,17]],"date-time":"2022-02-17T00:00:00Z","timestamp":1645056000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100001250","name":"Morris Animal Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001250","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Vet. Sci."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Duchenne muscular dystrophy (DMD) is an X-linked inherited myopathy that causes progressive skeletal and cardiac muscle disease. Heart lesions were described in the earliest DMD reports, and cardiomyopathy is now the leading cause of death. However, diagnostics and treatment for cardiomyopathy have lagged behind those for appendicular and respiratory skeletal muscle disease. Most animal model studies have been done in the mdx mouse, which has a relatively mild form of cardiomyopathy. Dogs with the genetically homologous condition, Golden Retriever muscular dystrophy (GRMD), develop progressive cardiomyopathy analogous to that seen in DMD. Previous descriptive studies of GRMD cardiomyopathy have mostly been limited to selective sampling of the hearts from young dogs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and Results<\/jats:title><jats:p>We systematically assessed cardiac lesions in 31 GRMD and carrier dogs aged 3 to 76 months and a separate cohort of 2\u201310-year-old normal hounds. Both semi-quantitative lesion scoring and quantitation of the cross-sectional area of fibrosis distinguished dogs with GRMD disease from normal dogs. The carriers generally had intermediate involvement but had even greater fibrosis than GRMD dogs. Fatty infiltration was the most prominent feature in some older GRMD dogs. Vascular hypertrophy was increased in GRMD dogs and correlated positively with lesion severity. Purkinje fiber vacuolation was also increased but did not correlate with lesion severity. Histopathologic changes correlated with late gadolinium enhancement on cardiac MRI.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These features are generally compatible with those of DMD and further validate GRMD as a useful model to study cardiomyopathy pathogenesis and treatment. Additionally, the nature of some degenerative lesions suggests that functional hypoxia or non-thrombotic ischemia may contribute to disease progression.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fvets.2021.759585","type":"journal-article","created":{"date-parts":[[2022,2,17]],"date-time":"2022-02-17T10:59:58Z","timestamp":1645095598000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Natural History of Histopathologic Changes in Cardiomyopathy of Golden Retriever Muscular Dystrophy"],"prefix":"10.3389","volume":"8","author":[{"given":"Sarah M.","family":"Schneider","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Garett T.","family":"Sansom","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee-Jae","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinji","family":"Furuya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brad R.","family":"Weeks","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joe N.","family":"Kornegay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,2,17]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"352","DOI":"10.1002\/ajmg.1320420320","article-title":"Canine X-linked muscular dystrophy as an animal model of Duchenne muscular dystrophy: a review","volume":"42","author":"Valentine","year":"1992","journal-title":"Am J Mol Genet."},{"key":"B2","doi-asserted-by":"publisher","first-page":"85","DOI":"10.1007\/s00335-011-9382-y","article-title":"Canine models of Duchenne muscular dystrophy and their use in therapeutic strategies","volume":"23","author":"Kornegay","year":"2012","journal-title":"Mamm Genome."},{"key":"B3","doi-asserted-by":"publisher","first-page":"919","DOI":"10.1016\/0092-8674(87)90579-4","article-title":"Dystrophin: the protein product of the duchenne muscular dystrophy locus","volume":"51","author":"Hoffman","year":"1987","journal-title":"Cell."},{"key":"B4","doi-asserted-by":"publisher","first-page":"375","DOI":"10.1016\/S0046-8177(76)80053-6","article-title":"The pathology of the heart in progressive muscular dystrophy: epimyocardial fibrosis","volume":"7","author":"Frankel","year":"1976","journal-title":"Hum Pathol."},{"key":"B5","doi-asserted-by":"publisher","first-page":"283","DOI":"10.1016\/0002-8703(78)90358-7","article-title":"Sequence of cardiac changes in Duchenne muscular dystrophy","volume":"95","author":"Heymsfield","year":"1978","journal-title":"Am Heart J."},{"key":"B6","doi-asserted-by":"publisher","first-page":"8","DOI":"10.1002\/mus.22097","article-title":"Cardiomyopathy of duchenne muscular dystrophy: current understanding and future directions","volume":"44","author":"Spurney","year":"2011","journal-title":"Muscle Nerve."},{"key":"B7","doi-asserted-by":"publisher","first-page":"1440","DOI":"10.1126\/science.1202768","article-title":"X-ROS signaling: rapid mechano-chemo transduction in heart","volume":"333","author":"Prosser","year":"2011","journal-title":"Science."},{"key":"B8","doi-asserted-by":"publisher","first-page":"E2905","DOI":"10.1073\/pnas.1402544111","article-title":"Impaired functional communication between the L-type calcium channel and mitochondria contributes to metabolic inhibition in the mdx heart","volume":"111","author":"Viola","year":"2014","journal-title":"Proc Natl Acad Sci."},{"key":"B9","doi-asserted-by":"publisher","first-page":"114","DOI":"10.1016\/j.ceca.2009.06.002","article-title":"Pathways of abnormal stress-induced Ca2+ influx into dystrophic mdx cardiomyocytes","volume":"46","author":"Fanchaouy","year":"2009","journal-title":"Cell Calcium."},{"key":"B10","doi-asserted-by":"publisher","first-page":"21","DOI":"10.1186\/s12920-017-0257-2","article-title":"GRMD cardiac and skeletal muscle metabolism gene profiles are distinct","volume":"10","author":"Markham","year":"2017","journal-title":"BMC Med Genom."},{"key":"B11","doi-asserted-by":"publisher","first-page":"349","DOI":"10.1161\/01.RES.72.2.349","article-title":"Dystrophin-glycoprotein complex and laminin colocalize to the sarcolemma and transverse tubules of cardiac muscle","volume":"72","author":"Klietsch","year":"1993","journal-title":"Circ Res."},{"key":"B12","doi-asserted-by":"publisher","first-page":"2501","DOI":"10.1006\/jmcc.1996.9999","article-title":"Dystrophin\u2013glycoprotein complex purified from hamster cardiac muscle. 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