{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T21:10:39Z","timestamp":1768511439678,"version":"3.49.0"},"posted":{"date-parts":[[2024,4,20]]},"group-title":"Physiology","reference-count":70,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,4,20]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Cardiomyopathy is the leading cause of death in Duchenne muscular dystrophy (DMD), however, in the\n                  <jats:italic>mdx<\/jats:italic>\n                  mouse model of DMD, the cardiac phenotype differs from that seen in DMD-associated cardiomyopathy. Although some have used pharmacologic stress to enhance the cardiac phenotype in the\n                  <jats:italic>mdx<\/jats:italic>\n                  model, many methods lead to high mortality, variable cardiac outcomes, and do not recapitulate the structural and functional cardiac changes seen in human disease. Here, we describe a simple and effective method to enhance the cardiac phenotype model in\n                  <jats:italic>mdx<\/jats:italic>\n                  mice using advanced 2D and 4D high-frequency ultrasound to monitor cardiac dysfunction progression\n                  <jats:italic>in vivo<\/jats:italic>\n                  . For our study,\n                  <jats:italic>mdx<\/jats:italic>\n                  and wild-type (WT) mice received daily low-dose (2 mg\/kg\/day) isoproterenol injections for 10 days. Histopathologic assessment showed that isoproterenol treatment increased myocyte injury, elevated serum cardiac troponin I levels, and enhanced fibrosis in\n                  <jats:italic>mdx<\/jats:italic>\n                  mice. Ultrasound revealed reduced ventricular function, decreased wall thickness, increased volumes, and diminished cardiac reserve in mdx mice compared to wild-type. Our findings highlight the utility of low-dose isoproterenol in\n                  <jats:italic>mdx<\/jats:italic>\n                  mice as a valuable model for exploring therapies targeting DMD-associated cardiac complications.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>SUMMARY STATEMENT<\/jats:title>\n                  <jats:p>This work introduces an improved method to model heart failure in mouse models of Duchenne muscular dystrophy and comprehensively describes underlying cellular and physiologic mechanisms using advanced imaging techniques.<\/jats:p>\n                <\/jats:sec>","DOI":"10.1101\/2024.04.15.589650","type":"posted-content","created":{"date-parts":[[2024,4,20]],"date-time":"2024-04-20T23:18:01Z","timestamp":1713655081000},"source":"Crossref","is-referenced-by-count":0,"title":["Functional cardiac consequences of \u03b2-adrenergic stress-induced injury in the\n                  <i>mdx<\/i>\n                  mouse model of Duchenne muscular dystrophy"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7916-3165","authenticated-orcid":false,"given":"Conner C.","family":"Earl","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9056-9887","authenticated-orcid":false,"given":"Areli J.","family":"Javier","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alyssa M.","family":"Richards","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2804-4641","authenticated-orcid":false,"given":"Larry W.","family":"Markham","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8883-7953","authenticated-orcid":false,"given":"Craig 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