{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T08:05:19Z","timestamp":1789718719201,"version":"4.0.1"},"reference-count":41,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T00:00:00Z","timestamp":1787184000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T00:00:00Z","timestamp":1787184000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"publisher","award":["23141901500"],"award-info":[{"award-number":["23141901500"]}],"id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100008750","name":"Shanghai Municipal Hospital Development Center","doi-asserted-by":"publisher","award":["SHDC22023302"],"award-info":[{"award-number":["SHDC22023302"]}],"id":[{"id":"10.13039\/501100008750","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>\n                    Hypertrophic Cardiomyopathy (HCM) is one of the significant causes of heart failure. This study aimed to identify and validate potential therapeutic targets for HCM through bioinformatics analysis and in\u00a0vitro and in\u00a0vivo experiments. By analysing differentially expressed genes in HCM patients and combining multiple analytical approaches, key genes were screened. The functions of these genes were validated using AC16 cells under different mechanical force environments and Ang\u2014II induction. HCM\u2010like pathological cardiac remodelling mouse model was established to evaluate myocardial hypertrophy, fibrosis and cardiac remodelling. The results demonstrated that\n                    <jats:italic>DUSP1<\/jats:italic>\n                    expression was downregulated in the myocardium of HCM patients. Mechanical force transduction activated the MAPK pathway and overexpression of DUSP1 suppressed ERK\/MAPK activation and attenuated mechanotransduction\u2010associated cardiomyocyte hypertrophy and hypertrophic gene expression. In\u00a0vivo experiments showed that cardiac\u2010specific restoration of DUSP1 expression alleviated pathological cardiac remodelling and fibrosis. This study suggests that DUSP1 functions as an endogenous regulator of mechanically activated MAPK signalling, thereby limiting pathological myocardial hypertrophy. These findings identify a previously underappreciated role of DUSP1 in linking mechanical stress\u2010induced signalling with MAPK activation and pathological cardiac remodelling, suggesting DUSP1 restoration as a potential therapeutic strategy for HCM\u2010like cardiac remodelling.\n                  <\/jats:p>","DOI":"10.1111\/1440-1681.70152","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T05:30:41Z","timestamp":1787290241000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>DUSP1<\/scp>\n                    Inhibits Mechanotransduction and\n                    <scp>MAPK<\/scp>\n                    Signalling to Alleviate Myocardial Cell Hypertrophy"],"prefix":"10.1111","volume":"53","author":[{"given":"Xiao","family":"Zhong","sequence":"first","affiliation":[{"name":"Department of Cardiology Huadong Hospital, Fudan University  Shanghai 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