{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T14:06:29Z","timestamp":1792073189132,"version":"4.4.0"},"reference-count":37,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2021,8,23]],"date-time":"2021-08-23T00:00:00Z","timestamp":1629676800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004480","name":"Natural Science Foundation of Shanxi Province","doi-asserted-by":"publisher","award":["201601D011111"],"award-info":[{"award-number":["201601D011111"]}],"id":[{"id":"10.13039\/501100004480","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiac hypertrophy has been a high prevalence rate throughout the world. It has posed a big threat to public health due to limited therapeutic approaches. Previous studies showed that pathological cardiac hypertrophy was associated with autophagy, microRNAs (miRNA), and other signaling pathways, while the molecular mechanisms remain incompletely characterized. In this study, we used thoracic aortic constriction (TAC)\u2010induced mice and angiotensin\u2010II (Ang\u2010II)\u2010induced H9C2 cell line as cardiac hypertrophy model to investigate the role of miR\u201026a\u20105p in cardiac hypertrophy. We found that miR\u201026a\u20105p was downregulated in cardiac hypertrophy mice. Overexpression of miR\u201026a\u20105p by type 9 recombinant adeno\u2010associated virus (rAAV9) reversed the heart hypertrophic manifestations. The phenotypes were also promoted by miR\u201026a\u20105p inhibitor in Ang\u2010II\u2010induced H9C2 cells. Through miRNA profile analysis and dual\u2010luciferase reporter assay, ADAM17 was identified as a direct target of miR\u201026a\u20105p. Restored expression of ADAM17 disrupted the effect of miR\u201026a\u20105p on cardiac hypertrophy. To sum up, these results indicated that miR\u201026a\u20105p played an inhibitory role in cardiac hypertrophy and dysfunction via targeting ADAM17. The miR\u201026a\u20105p\u2010ADAM17\u2010cardiac hypertrophy axis provided special insight and a new molecular mechanism for a better understanding of cardiac hypertrophy disease, as well as the diagnostic and therapeutic practice.<\/jats:p>","DOI":"10.1002\/cbin.11685","type":"journal-article","created":{"date-parts":[[2021,8,9]],"date-time":"2021-08-09T19:43:59Z","timestamp":1628538239000},"page":"2357-2367","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["MiR\u201026a\u20105p alleviates cardiac hypertrophy and dysfunction via targeting ADAM17"],"prefix":"10.1002","volume":"45","author":[{"given":"Hongtao","family":"Shi","sequence":"first","affiliation":[{"name":"Department of Cardiology The First Hospital of Shanxi Medical University Taiyuan Shanxi PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology 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