{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T04:13:30Z","timestamp":1790050410193,"version":"4.0.1"},"reference-count":40,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,12,13]],"date-time":"2012-12-13T00:00:00Z","timestamp":1355356800000},"content-version":"vor","delay-in-days":12,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Progressive cardiomyopathy is a major cause of death in Duchenne muscular dystrophy (<jats:styled-content style=\"fixed-case\">DMD<\/jats:styled-content>) patients. Coupling between <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup> handling and contractile properties in dystrophic hearts is poorly understood. It is also not clear whether developing cardiac failure is dominated by alterations in <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup> pathways or more related to the contractile apparatus. We simultaneously recorded force and <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup> transients in field\u2010stimulated papillary muscles from young (10\u201314\u00a0weeks) wild\u2010type (wt) and dystrophic mdx mice. Force amplitudes were fivefold reduced in mdx muscles despite only 30\u00a0% reduction in fura\u20102 ratio amplitudes. This indicated mechanisms other than systolic <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup> to additionally account for force decrements in mdx muscles. p<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content>\u2010force relations revealed decreased mdx myofibrillar <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup> sensitivity. \u2018<jats:italic>In vitro<\/jats:italic>\u2019 motility assays, studied in mdx hearts here for the first time, showed significantly slower sliding velocities. mdx <jats:styled-content style=\"fixed-case\">MLC<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content> isoforms were not grossly altered. Dystrophic hearts showed echocardiography signs of early ventricular wall hypertrophy with a significantly enlarged end\u2010diastolic diameter \u2018<jats:italic>in vivo<\/jats:italic>\u2019. However, fractional shortening was still comparable to wt mice. Changes in the contractile apparatus satisfactorily explained force drop in mdx hearts. We give first evidence of early hypertrophy in mdx mice and possible mechanisms for already functional impairment of cardiac muscle in <jats:styled-content style=\"fixed-case\">DMD<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2012.01630.x","type":"journal-article","created":{"date-parts":[[2012,9,13]],"date-time":"2012-09-13T11:17:10Z","timestamp":1347535030000},"page":"3028-3036","source":"Crossref","is-referenced-by-count":16,"title":["The heart in Duchenne muscular dystrophy: early detection of contractile performance alteration"],"prefix":"10.1111","volume":"16","author":[{"given":"S\u00f6ren","family":"Wagner","sequence":"first","affiliation":[{"name":"Department of Anesthesiology University of Heidelberg Heidelberg Germany"},{"name":"Department of cardio\u2010thoracic surgery University of Essen Essen Germany"},{"name":"Institute of Physiology &amp; Pathophysiology Department of Systems Physiology University of Heidelberg Heidelberg Germany"},{"name":"Department 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