{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T08:04:53Z","timestamp":1789718693303,"version":"4.0.1"},"reference-count":40,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T00:00:00Z","timestamp":1788048000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T00:00:00Z","timestamp":1788048000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81670383"],"award-info":[{"award-number":["81670383"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82370438"],"award-info":[{"award-number":["82370438"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Heat shock factor 2 (HSF2) and hypoxia\u2010inducible factor 1\u03b1 are activated by angiotensin II (ANGII) in cardiomyocytes. The endoplasmic reticulum (ER) stress plays a critical role in cardiac hypertrophy. Moreover, HIF\u20101\u03b1 is known to be regulated by HSF2 in tumour cells. In this study, we hypothesised and clarified whether HSF2 trans\u2010activated HIF\u20101\u03b1 through initiation of ER stress in hypertrophic cardiomyocytes. Myocardial hypertrophy was induced by the treatment of ANGII. Expression of the gene or protein was assessed by applying RT\u2010PCR, WB, ICC and IHC. Luciferase and CHIP were applied to detect the transcription of HIF\u20101\u03b1 by HSF2. Both in\u00a0vitro and in\u00a0vivo, the expression of HIF\u20101\u03b1, ER stress markers and HSF2 was increased in ANGII\u2010treated hypertrophic cardiomyocytes. Blocking ER stress suppressed the expression of HSF2 and HIF\u20101\u03b1 in ANGII\u2010treated cardiomyocytes. Silencing HSF2 inhibited HIF\u20101\u03b1, thereby reducing hypertrophy but had no effect on ER stress. Similarly, silencing HIF\u20101\u03b1 reduced hypertrophy without affecting ER stress or HSF2 expression. HSF2 transcriptionally activated HIF\u20101\u03b1. We concluded that ER stress induced by ANGII activates HSF2, which then trans\u2010activates HIF\u20101\u03b1, promoting cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/1440-1681.70153","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T02:36:52Z","timestamp":1788143812000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>ANGII<\/scp>\n                    Initiated\n                    <scp>HSF2<\/scp>\n                    Trans\u2010Activating\n                    <scp>HIF<\/scp>\n                    \u20101\u03b1 Through Induction of\n                    <scp>ER<\/scp>\n                    Stress to Promote Cardiac Hypertrophy"],"prefix":"10.1111","volume":"53","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1406-489X","authenticated-orcid":false,"given":"Renchuang","family":"Cao","sequence":"first","affiliation":[{"name":"Department of Physiology Dalian Medical 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