{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T06:51:43Z","timestamp":1787727103851,"version":"build-2784847793"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,1,3]],"date-time":"2019-01-03T00:00:00Z","timestamp":1546473600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100010722","name":"Harbin Medical University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010722","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction. Nevertheless, the pathophysiological mechanisms of cardiac hypertrophy have never been elucidated. Recent studies indicated that miR\u2010103 expression was significantly decreased in heart failure patients. However, less is known about the role of miR\u2010103 in cardiac hypertrophy. The present study was designed to investigate the relationship between miR\u2010103 and the mechanism of pressure overload\u2010induced cardiac hypertrophy. <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 protein, cardiac hypertrophy marker proteins (<jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content> and \u03b2\u2010<jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content>) and autophagy associated proteins (Beclin\u20101 and <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>) were up\u2010regulated, as well as, miR\u2010103 expression and autophagy associated proteins (p62) were down\u2010regulated in cardiac hypertrophy models in\u00a0vivo and in\u00a0vitro respectively. Further results indicated that silencing <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 or forcing overexpression of miR\u2010103 could dramatically inhibit cell surface area, relative fluorescence intensity of Ca<jats:sup>2+<\/jats:sup> signal and the expressions of <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>, \u03b2\u2010<jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content>, Beclin\u20101 and <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>, but promote p62 expression. Moreover, <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 protein was decreased in neonatal rat ventricular myocyte transfected with miR\u2010103, but increased by <jats:styled-content style=\"fixed-case\">AMO<\/jats:styled-content>\u2010103. Co\u2010transfection of the miR\u2010103 with the luciferase reporter vector into <jats:styled-content style=\"fixed-case\">HEK<\/jats:styled-content>293 cells caused a sharp decrease in luciferase activity compared with transfection of the luciferase vector alone. The miR\u2010103\u2010induced depression of luciferase activity was rescued by an <jats:styled-content style=\"fixed-case\">AMO<\/jats:styled-content>\u2010103. These findings suggested that <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 was a direct target of miR\u2010103. In conclusion, miR\u2010103 could attenuate cardiomyocyte hypertrophy partly by reducing cardiac autophagy activity through the targeted inhibition of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 signalling in the pressure\u2010overloaded rat hearts.<\/jats:p>","DOI":"10.1111\/jcmm.14095","type":"journal-article","created":{"date-parts":[[2019,1,3]],"date-time":"2019-01-03T08:06:15Z","timestamp":1546502775000},"page":"1926-1939","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["MiR\u2010103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting <scp>TRPV<\/scp>3 channel in rat hearts"],"prefix":"10.1111","volume":"23","author":[{"given":"Hanping","family":"Qi","sequence":"first","affiliation":[{"name":"Department of Pharmacology Harbin Medical University\u2010Daqing Daqing 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