{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T02:32:58Z","timestamp":1787884378295,"version":"build-2784847793"},"reference-count":53,"publisher":"Wiley","issue":"22","license":[{"start":{"date-parts":[[2023,8,21]],"date-time":"2023-08-21T00:00:00Z","timestamp":1692576000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82060046"],"award-info":[{"award-number":["82060046"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2023,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Pathological myocardial remodelling is the initial factor of chronic heart failure (CHF) and is induced by multiple factors. We previously demonstrated that histone acetylation is involved in CHF in transverse aortic constriction (TAC) mice, a model for pressure overload\u2010induced heart failure. In this study, we investigated whether the histone deacetylase Sirtuin 6 (SIRT6), which mediates deacetylation of histone 3 acetylated at lysine 9 (H3K9ac), is involved pathological myocardial remodelling by regulating myocardial energy metabolism and explored the underlying mechanisms. We generated a TAC mouse model by partial thoracic aortic banding. TAC mice were injected with the SIRT6 agonist MDL\u2010800 at a dose of 65\u2009mg\/kg for 8\u2009weeks. At 4, 8 and 12\u2009weeks after TAC, the level of H3K9ac increased gradually, while the expression of SIRT6 and vascular endothelial growth factor A (VEGFA) decreased gradually. MDL\u2010800 reversed the effects of SIRT6 on H3K9ac in TAC mice and promoted the expression of VEGFA in the hearts of TAC mice. MDL\u2010800 also attenuated mitochondria damage and improved mitochondrial respiratory function through upregulating SIRT6 in the hearts of TAC mice. These results revealed a novel mechanism in which SIRT6\u2010mediated H3K9ac level is involved pathological myocardial remodelling in TAC mice through regulating myocardial energy metabolism. These findings may assist in the development of novel methods for preventing and treating pathological myocardial remodelling.<\/jats:p>","DOI":"10.1111\/jcmm.17915","type":"journal-article","created":{"date-parts":[[2023,8,22]],"date-time":"2023-08-22T05:25:58Z","timestamp":1692681958000},"page":"3451-3464","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["<scp>SIRT6<\/scp> mediated histone <scp>H3K9ac<\/scp> deacetylation involves myocardial remodelling through regulating myocardial energy metabolism in <scp>TAC<\/scp> mice"],"prefix":"10.1111","volume":"27","author":[{"given":"Shuqi","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Guizhou Children's Hospital Affiliated Hospital of Zunyi Medical University  Zunyi Guizhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaojiao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of 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