{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:27:51Z","timestamp":1791329271085,"version":"4.3.1"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Transposition of the great arteries is one of the most commonly diagnosed conotruncal heart defects at birth, but its etiology is largely unknown. The anterior heart field (\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              ) that resides in the anterior pharyngeal arches contributes to conotruncal development, during which heart progenitors that originated from the left and right\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              migrate to form distinct conotruncal regions. The aim of this study is to identify abnormal AHF development that causes the morphology of transposition of the great arteries.\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 placed a retinoic acid\u2013soaked bead on the left or the right or on both sides of the\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              of stage 12 to 14 chick embryos and examined the conotruncal heart defect at stage 34. Transposition of the great arteries was diagnosed at high incidence in embryos for which a retinoic acid\u2013soaked bead had been placed in the left\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              at stage 12. Fluorescent dye tracing showed that\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              exposed to retinoic acid failed to contribute to conotruncus development.\n              <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n              8 and Isl1 expression were downregulated in retinoic acid\u2013exposed\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              , and differentiation and expansion of cardiomyocytes were suppressed in cultured\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              in medium supplemented with retinoic acid.\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 left\n              <jats:styled-content style=\"fixed-case\">AHF<\/jats:styled-content>\n              at the early looped heart stage, corresponding to Carnegie stages 10 to 11 (28 to 29\u00a0days after fertilization) in human embryos, is the region of the impediment that causes the morphology of transposition of the great arteries.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.115.001889","type":"journal-article","created":{"date-parts":[[2015,5,1]],"date-time":"2015-05-01T01:12:28Z","timestamp":1430442748000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":14,"title":["Impaired Development of Left Anterior Heart Field by Ectopic Retinoic Acid Causes Transposition of the Great Arteries"],"prefix":"10.1161","volume":"4","author":[{"given":"Mayu","family":"Narematsu","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology Graduate School of Medicine Osaka City University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuya","family":"Kamimura","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology Graduate School of Medicine Osaka City University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiyuki","family":"Yamagishi","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology Graduate School of Medicine Osaka City University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitsuru","family":"Fukui","sequence":"additional","affiliation":[{"name":"Laboratory of Statics Graduate School of Medicine Osaka City University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuji","family":"Nakajima","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology Graduate School of Medicine Osaka City University Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(02)01886-7"},{"key":"e_1_3_2_3_2","first-page":"639","volume-title":"Developmental Mechanisms of Heart Disease","author":"Ferencz C","year":"1995","unstructured":"Ferencz C, Brenner JI, Loffredo C, Kappetein AP, Wilson PD. 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