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Regression of cardiac hypertrophy has emerged as a promising strategy in the treatment of <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> patients. Here, we have been suggested that heat\u2010shock transcription factor 1 (<jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1) is a novel repressor of ischaemia\u2010induced cardiac hypertrophy. Ligation of left anterior descending coronary was used to produce <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1\u2010deficient heterozygote (<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>), <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 transgenic (<jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content>) mice and their wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) littermates, respectively. Neonatal rat cardiomyocytes (<jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>s) were treated by hypoxia to mimic <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> in vitro. The <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 phosphorylation was significantly reduced in the infarct border zone of mouse left ventricles (<jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content>s) 1 week after <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> and in the hypoxia\u2010treated <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice showed more significant maladaptive cardiac hypertrophy and deteriorated cardiac dysfunction 1 week after <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> compared to <jats:styled-content style=\"fixed-case\">WT MI<\/jats:styled-content> mice. Deficiency of <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 by si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> transfection notably increased the hypoxia\u2010induced myocardial hypertrophy in <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>s. Mechanistically, Janus kinase 2 (<jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2) and its effector, signal transducer and activator of transcription 3 (<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3) were found to be significantly increased in the <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> infarct border zone of <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice after <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> as well as the <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>s treated by hypoxia. These alterations were more significant in <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice and <jats:styled-content style=\"fixed-case\">NRCM<\/jats:styled-content>s transfected with <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 Si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>. Inversely, <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 <jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content> mice showed significantly ameliorated cardiac hypertrophy and heart failure 1 week after <jats:styled-content style=\"fixed-case\">LAD<\/jats:styled-content> ligation compared to their <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> littermates. Our data collectively demonstrated that <jats:styled-content style=\"fixed-case\">HSF<\/jats:styled-content>1 is critically involved in the pathological cardiac hypertrophy after <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> via modulating <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3 signalling and may constitute a potential therapeutic target for <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> patients.<\/jats:p>","DOI":"10.1111\/jcmm.13713","type":"journal-article","created":{"date-parts":[[2018,7,11]],"date-time":"2018-07-11T07:16:24Z","timestamp":1531293384000},"page":"4292-4303","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Heat\u2010shock transcription factor 1 is critically involved in the ischaemia\u2010induced cardiac hypertrophy via <scp>JAK<\/scp>2\/<scp>STAT<\/scp>3 pathway"],"prefix":"10.1111","volume":"22","author":[{"given":"Lingyan","family":"Yuan","sequence":"first","affiliation":[{"name":"Department of kinesiology Institute of physical education Shanghai Normal University Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Qiu","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yong","family":"Ye","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital and Institutes of Biological Science Fudan University Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jian","family":"Wu","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital and Institutes 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