CCAAT/enhancer-binding protein β overexpression alleviates myocardial remodelling by regulating angiotensin-converting enzyme-2 expression in diabetes.

摘要: Diabetic cardiomyopathy, a major cardiac complication, contributes to heart remodelling and failure. Our previous study discovered that CCAAT/enhancer-binding protein β (C/EBPβ), transcription factor belongs family of basic leucine zipper factors, interacts with the angiotensin-converting enzyme 2 (ACE2) promoter sequence in other disease models. Here, we aimed determine role C/EBPβ diabetes whether ACE2 expression is regulated by C/EBPβ. A type 1 diabetic mouse model was generated an intraperitoneal injection streptozotocin. mice were injected lentivirus expressing either or sh-C/EBPβ treated valsartan after 12 weeks observe effects In vitro, fibroblasts cardiomyocytes high glucose (HG) investigate anti-fibrosis, anti-apoptosis regulatory mechanisms down-regulated HG-induced neonatal cells. overexpression significantly attenuated collagen deposition cardiomyocyte apoptosis up-regulating expression. The molecular mechanism involved binding sequence. Although valsartan, classic angiotensin receptor blocker, relieved complications, up-regulation may exert greater beneficial on patients cardiomyopathy.