{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T13:35:51Z","timestamp":1782480951412,"version":"3.54.5"},"reference-count":23,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2015,3,8]],"date-time":"2015-03-08T00:00:00Z","timestamp":1425772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81000072, 81001683"],"award-info":[{"award-number":["81000072, 81001683"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>This study was designed to investigate the expression of short\u2010chain acyl\u2010CoA dehydrogenase (<jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content>), a key enzyme of fatty acid \u03b2\u2010oxidation, during rat heart development and the difference of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> between pathological and physiological cardiac hypertrophy. The expression of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> was lowest in the foetal and neonatal heart, which had time\u2010dependent increase during normal heart development. In contrast, a significant decrease in <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> expression was observed in different ages of spontaneously hypertensive rats (<jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content>). On the other hand, swim\u2010trained rats developed physiological cardiac hypertrophy, whereas <jats:styled-content style=\"fixed-case\">SHR<\/jats:styled-content> developed pathological cardiac hypertrophy. The two kinds of cardiac hypertrophy exhibited divergent <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> changes in myocardial fatty acids utilization. In addition, the expression of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> was significantly decreased in pathological cardiomyocyte hypertrophy, however, increased in physiological cardiomyocyte hypertrophy. <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> treatment triggered the pathological cardiomyocyte hypertrophy, which showed that the down\u2010regulation of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> expression may play an important role in pathological cardiac hypertrophy. The changes in peroxisome proliferator\u2010activated receptor \u03b1 (<jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b1) was accordant with that of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content>. Moreover, the specific <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b1 ligand fenofibrate treatment increased the expression of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> and inhibited pathological cardiac hypertrophy. Therefore, we speculate that the down\u2010regulated expression of <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> in pathological cardiac hypertrophy may be responsible for \u2018the recapitulation of foetal energy metabolism\u2019. The deactivation of <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b1 may result in the decrease in <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> expression in pathological cardiac hypertrophy. Changes in <jats:styled-content style=\"fixed-case\">SCAD<\/jats:styled-content> are different in pathological and physiological cardiac hypertrophy, which may be used as the molecular markers of pathological and physiological cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/jcmm.12541","type":"journal-article","created":{"date-parts":[[2015,3,9]],"date-time":"2015-03-09T02:05:15Z","timestamp":1425866715000},"page":"1672-1688","source":"Crossref","is-referenced-by-count":17,"title":["Changes in short\u2010chain acyl\u2010coA dehydrogenase during rat cardiac development and stress"],"prefix":"10.1111","volume":"19","author":[{"given":"Jinxian","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacy GuangDong Pharmaceutical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lipeng","family":"Xu","sequence":"additional","affiliation":[{"name":"Institute of New Drug Research and Guangdong Province Key Laboratory of 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