title: MicroRNA-497 Inhibits Cardiac Hypertrophy by Targeting Sirt4.
abstract: Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin Ⅱ (Ang Ⅱ) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.
authors.affiliation: Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.|Department of Cardiovascular Surgery, Shanghai Yodak Cardiothracic Hospital, Shanghai, China.
authors.forename: Yimin
authors.initials: Y
authors.lastname: Xiao
authors.affiliation: Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.|Department of Cardiovascular Surgery, Shanghai Yodak Cardiothracic Hospital, Shanghai, China.
authors.forename: Xiaofei
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.|Department of Cardiovascular Surgery, Shanghai Yodak Cardiothracic Hospital, Shanghai, China.
authors.forename: Shihao
authors.initials: S
authors.lastname: Fan
authors.affiliation: Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.
authors.forename: Guanghao
authors.initials: G
authors.lastname: Cui
authors.affiliation: Department of Cardiovascular Surgery of the First Affiliated Hospital & Institute for Cardiovascular Science, Soochow University, Suzhou, China.
authors.forename: Zhenya
authors.initials: Z
authors.lastname: Shen
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000235:genetics*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D015971:Gene Expression Regulation, Enzymologic; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000502:physiology*; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism; D037761:Sirtuins / Q000235:genetics* / Q000378:metabolism
chemical_list: D035683:MicroRNAs; D024101:Mitochondrial Proteins; C550139:mirn497 microRNA, mouse; C514813:SIRT4 protein, mouse; D037761:Sirtuins