Pressure overload induced heart failure is profoundly attenuated by deletion of the translational re

• 作 者: ZhongbingLu[1]XinliHu[2]XinXu[2]PingZhang[2]RobertJ.Bache[2]YingjieChen[2]
• 机 构: College of Life Sciences, Graduate University of Chinese Academy of Science,19A Yuquanlu,Beijing,Chi
• 出 处: 第七届中国科学院“百人学者论坛”学术年会
• 发表日期: 2012年期

　　Assembly of the translation initiation machinery is negatively regulated by the eukaryotic translation initiation factor 4E binding proteins, which sequester the mRNA cap-binding protein eIF4E, thus preventing assembly of an intact initiation complex. However, the role of translational control on the development of congestive heart failure (CHF) has not been systematically examined. Here we perturbed translational control in mice by knockout of both 4E binding protein 1 (Eif4ebp1) and 2 (Eif4ebp2) (designated as Eif4ebp1/2 double knockout) to study its impact on left ventricular hypertrophy and CHF resulting from transverse aortic constriction. Eif4ebp1/2 double knockout caused a modest increase in left ventricular mass under basal conditions. However, following transverse aortic constriction, Eif4ebp1/2 double knockout profoundly attenuated the development of CHF and its attendant mortality.