{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T14:11:57Z","timestamp":1791987117167,"version":"4.4.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"15","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,8,6]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In mammals, muscle contraction is controlled by a family of 10 sarcomeric myosin motors. The expression of one of its members,\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b, is regulated by alternative splicing, and while the protein is restricted to specialized muscles such as extraocular muscles or muscle spindles,\n              <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n              that cannot encode protein is expressed in most skeletal muscles and in the heart. Remarkably, birds and snakes express\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b protein in both heart and skeletal muscles. This observation suggests that in the mammalian heart, the motor activity of\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b may only be needed during development since its expression is prevented in adult tissue, possibly because it could promote disease by unbalancing myocardial contractility.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We have analyzed\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b null mice to determine the potential role of\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b during cardiac development and also generated transgenic mice with cardiac myocyte expression of\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b protein to measure its impact on cardiomyocyte function and contractility. We found that\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b null mice are born at expected Mendelian ratios and do not have a baseline cardiac phenotype as adults. In contrast, transgenic cardiac\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b protein expression induced early cardiac dilation in males with significantly increased left ventricular mass in both sexes. Cardiac dilation is progressive, leading to early cardiac dysfunction in males, but later dysfunction in females.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The data presented show that the expression of\n              <jats:styled-content style=\"fixed-case\">MYH<\/jats:styled-content>\n              7b protein in the mammalian heart has been inhibited during the evolution of mammals most likely to prevent the development of a severe cardiomyopathy that is sexually dimorphic.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.013318","type":"journal-article","created":{"date-parts":[[2019,7,31]],"date-time":"2019-07-31T09:16:25Z","timestamp":1564564585000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":21,"title":["Expression of Normally Repressed Myosin Heavy Chain 7b in the Mammalian Heart Induces Dilated Cardiomyopathy"],"prefix":"10.1161","volume":"8","author":[{"given":"Angela K.","family":"Peter","sequence":"first","affiliation":[{"name":"Department of Molecular, Cellular and Developmental Biology Biofrontiers Institute University of Colorado Boulder CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alberto C.","family":"Rossi","sequence":"additional","affiliation":[{"name":"Department of Molecular, Cellular and Developmental Biology Biofrontiers Institute University of Colorado Boulder CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Massimo","family":"Buvoli","sequence":"additional","affiliation":[{"name":"Department of Molecular, Cellular and Developmental Biology Biofrontiers Institute University of Colorado Boulder CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher D.","family":"Ozeroff","sequence":"additional","affiliation":[{"name":"Department of Molecular, 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