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Our previous study discovered that <jats:styled-content style=\"fixed-case\">CCAAT<\/jats:styled-content>\/enhancer\u2010binding protein \u03b2 (C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2), a transcription factor that belongs to a family of basic leucine zipper transcription factors, interacts with the angiotensin\u2010converting enzyme 2 (<jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>2) promoter sequence in other disease models. Here, we aimed to determine the role of C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 in diabetes and whether <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>2 expression is regulated by C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2. A type 1 diabetic mouse model was generated by an intraperitoneal injection of streptozotocin. Diabetic mice were injected with a lentivirus expressing either C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 or sh\u2010C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 or treated with valsartan after 12 weeks to observe the effects of C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2. <jats:italic>In vitro<\/jats:italic>, cardiac fibroblasts and cardiomyocytes were treated with high glucose (<jats:styled-content style=\"fixed-case\">HG<\/jats:styled-content>) to investigate the anti\u2010fibrosis, anti\u2010apoptosis and regulatory mechanisms of C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2. C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 expression was down\u2010regulated in diabetic mice and <jats:styled-content style=\"fixed-case\">HG<\/jats:styled-content>\u2010induced cardiac neonatal cells. C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 overexpression significantly attenuated collagen deposition and cardiomyocyte apoptosis by up\u2010regulating <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>2 expression. The molecular mechanism involved the binding of C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 to the <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>2 promoter sequence. Although valsartan, a classic angiotensin receptor blocker, relieved diabetic complications, the up\u2010regulation of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>2 expression by C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 overexpression may exert greater beneficial effects on patients with diabetic cardiomyopathy.<\/jats:p>","DOI":"10.1111\/jcmm.13406","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T19:34:09Z","timestamp":1513884849000},"page":"1475-1488","source":"Crossref","is-referenced-by-count":17,"title":["<scp>CCAAT<\/scp>\/enhancer\u2010binding protein \u03b2 overexpression alleviates myocardial remodelling by regulating angiotensin\u2010converting enzyme\u20102 expression in 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