Suv39h1介导的SIRT1反式阻遏导致心脏缺血-再灌注损伤

SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury.
2017-04-19 11:42发表评论
作者:Guang Yang,Xinjian Zhang,Xinyu Weng,Peng Liang,Xin Dai,Sheng Zeng,Huihui Xu,Hailin Huan,Mingming Fang,Yuehua Li,Dachun Xu,Yong Xu
机构: 南京医科大学
期刊: BASIC RES CARDIOL 2017年5月21期112卷

Ischemic reperfusion (I/R) contributes to deleterious cardiac remodeling and heart failure. The deacetylase SIRT1 has been shown to protect the heart from I/R injury. We examined the mechanism whereby I/R injury represses SIRT1 transcription in the myocardium. There was accumulation of trimethylated histone H3K9 on the proximal SIRT1 promoter in the myocardium in mice following I/R injury and in cultured cardiomyocytes exposed to hypoxia–reoxygenation (H/R). In accordance, the H3K9 trimethyltransferase SUV39H1 bound to the SIRT1 promoter and repressed SIRT1 transcription. SUV39H1 expression was up-regulated in the myocardium in mice following I/R insults and in H/R-treated cardiomyocytes paralleling SIRT1 down-regulation. Silencing SUV39H1 expression or suppression of SUV39H1 activity erased H3K9Me3 from the SIRT1 promoter and normalized SIRT1 levels in cardiomyocytes. Meanwhile, SUV39H1 deficiency or inhibition attenuated I/R-induced infarction and improved heart function in mice likely through influencing ROS levels in a SIRT1-dependent manner. Therefore, our data uncover a novel mechanism for SIRT1 trans-repression during cardiac I/R injury and present SUV39H1 as a druggable target for the development of therapeutic strategies against ischemic heart disease.

通讯机构:Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of PathophysiologyNanjing Medical UniversityNanjingChina
学科代码:心血管病学   关键词:Suv39h1介导 SIRT1反式阻遏 心脏缺血 再灌注损伤 ,中国作者重要发表 爱思唯尔医学网, Elseviermed
来源: Scopus
Scopus介绍:Scopus 于2004年11月正式推出,是目前全球规模最大的文摘和引文数据库。Scopus涵盖了由5000多家出版商出版发行的科技、医学和社会科学方面的18,000多种期刊,其中同行评审期刊16,500多种。相对于其他单一的文摘索引数据库而言,Scopus的内容更加全面,学科更加广泛,特别是在获取欧洲及亚太地区的文献方面,用户可检索出更多的文献数量。通过Scopus,用户可以检索到1823年以来的近4000万条摘要和题录信息,以及1996年以来所引用的参考文献。数据每日更新。 马上访问Scopus网站http://www.scopus.com/
顶一下(0
您可能感兴趣的文章
发表评论网友评论(0)
发表评论
登录后方可发表评论,点击此处登录