{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T23:39:13Z","timestamp":1789774753247,"version":"4.0.1"},"reference-count":39,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2014,9,11]],"date-time":"2014-09-11T00:00:00Z","timestamp":1410393600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100002855","name":"Ministry of Science and Technology of the People's Republic of China","doi-asserted-by":"publisher","award":["2007DFC30340, 2010CB732601 and 2011BAI11B04"],"award-info":[{"award-number":["2007DFC30340, 2010CB732601 and 2011BAI11B04"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81070100 and 30700322"],"award-info":[{"award-number":["81070100 and 30700322"]}],"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":[[2014,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The molecular mechanisms that drive the development of cardiac hypertrophy in hypertrophic cardiomyopathy (\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    ) remain elusive. Accumulated evidence suggests that micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s are essential regulators of cardiac remodelling. We have been suggested that micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s could play a role in the process of\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    . To uncover which micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s were changed in their expression, micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    microarrays were performed on heart tissue from\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    patients (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a07) and from healthy donors (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a05). Among the 13 micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s that were differentially expressed in\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    , miR\u2010451 was the most down\u2010regulated. Ectopic overexpression of miR\u2010451 in neonatal rat cardiomyocytes (\n                    <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>\n                    ) decreased the cell size, whereas knockdown of endogenous miR\u2010451 increased the cell surface area. Luciferase reporter assay analyses demonstrated that tuberous sclerosis complex 1 (\n                    <jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>\n                    1) was a direct target of miR\u2010451. Overexpression of miR\u2010451 in both HeLa cells and\n                    <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>\n                    suppressed the expression of\n                    <jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>\n                    1. Furthermore,\n                    <jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>\n                    1 was significantly up\u2010regulated in\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    myocardia, which correlated with the decreased levels of miR\u2010451. As\n                    <jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>\n                    1 is a known positive regulator of autophagy, we examined the role of miR\u2010451 in the regulation of autophagy. Overexpression of miR\u2010451\n                    <jats:italic>in vitro<\/jats:italic>\n                    inhibited the formation of the autophagosome. Conversely, miR\u2010451 knockdown accelerated autophagosome formation. Consistently, an increased number of autophagosomes was observed in\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    myocardia, accompanied by up\u2010regulated autophagy markers, and the lipidated form of\n                    <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n                    3 and Beclin\u20101. Taken together, our findings indicate that miR\u2010451 regulates cardiac hypertrophy and cardiac autophagy by targeting\n                    <jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>\n                    1. The down\u2010regulation of miR\u2010451 may contribute to the development of\n                    <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content>\n                    and may be a potential therapeutic target for this disease.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.12380","type":"journal-article","created":{"date-parts":[[2014,9,11]],"date-time":"2014-09-11T04:19:12Z","timestamp":1410409152000},"page":"2266-2274","source":"Crossref","is-referenced-by-count":110,"title":["MiR\u2010451 is decreased in hypertrophic cardiomyopathy and regulates autophagy by targeting\n                    <scp>TSC<\/scp>\n                    1"],"prefix":"10.1111","volume":"18","author":[{"given":"Lei","family":"Song","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cardiovascular Diseases Fuwai Hospital National Center for Cardiovascular Disease Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Su","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Diseases Fuwai Hospital National Center for Cardiovascular Disease Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuiyun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Fuwai Hospital National Center for Cardiovascular Diseases Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yubao","family":"Zou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Cardiovascular Diseases Fuwai Hospital National Center for Cardiovascular Disease Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 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