The silencing transcription factor REST targets UCHL1 to regulate inflammatory response and fibrosis during cardiac hypertrophy  

作　　者：Wenze Cao Huan Liu Ye Xu Sangyu Hu Yujie Yang Li Li Luying Peng 

机构地区：[1]State Key Laboratory of Cardiology,Shanghai East Hospital,Tongji University School of Medicine,Shanghai 200120,China [2]Institute of Medical Genetics,Tongji University,Shanghai 200092,China [3]Heart Health Center,Shanghai East Hospital,Tongji University School of Medicine,Shanghai 200120,China [4]Department of Medical Genetics,Tongji University School of Medicine,Shanghai 200092,China [5]Research Units of Origin and Regulation of Heart Rhythm,Chinese Academy of Medical Sciences,Beijing 100730,China

出　　处：《Genes & Diseases》2024年第6期91-94,共4页基因与疾病（英文）

基　　金：supported by grants from the National Natural Science Foundation of China (No.32071109,82070-270,M-0048);the Shanghai Committee of Science and Technology (China) (No.21ZR1467000,22ZR1463800).

摘　　要：RE1 silencing transcription factor(REST)plays a key role in embryonic development and fetal cardiac gene reactivation.1 However,understanding of the role of REST in cardiac remodeling is very limited.A recent study has shown that cardiac-specific REST knockout increases Gao expression,and impairs Ca^(2+)processing in ventricular 1 myocytes,leading to cardiac dysfunction.

关 键 词：cardiac FETAL REST 

分 类 号：R542.2[医药卫生—心血管疾病]