Cardiac concentric hypertrophy promoted by activated Met receptor is mitigated in vivo by inhibition of Erk1,2 signalling with Pimasertib
作者: Valentina SalaSimona GalloStefano GattiEnzo MedicoElisa VignaDaniela CantarellaLara FontaniMassimo NataleJames CiminoMara MorelloPaolo Maria ComoglioAntonio PonzettoTiziana Crepaldi
作者单位: 1Department of Oncology, University of Turin, 10126 Turin, Italy
2Department of Medical Sciences, University of Turin, 10126 Turin, Italy
3FPO-IRCCS, 10060 Candiolo, TO, Italy
4Politecnico di Torino, 10129 Turin, Italy
5Department of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy
刊名: Journal of Molecular and Cellular Cardiology, 2016, Vol.93 , pp.84-97
来源数据库: Elsevier Journal
DOI: 10.1016/j.yjmcc.2016.02.017
关键词: Cardiac hypertrophyErk12Heart failureHGFRMet receptorMek1 inhibitor
原始语种摘要: Abstract(#br)Cardiac hypertrophy is a major risk factor for heart failure. Hence, its attenuation represents an important clinical goal. Erk1,2 signalling is pivotal in the cardiac response to stress, suggesting that its inhibition may be a good strategy to revert heart hypertrophy. In this work, we unveiled the events associated with cardiac hypertrophy by means of a transgenic model expressing activated Met receptor. c-Met proto-oncogene encodes for the tyrosine kinase receptor of Hepatocyte growth factor and is a strong inducer of Ras-Raf-Mek-Erk1,2 pathway. We showed that three weeks after the induction of activated Met, the heart presents a remarkable concentric hypertrophy, with no signs of congestive failure and preserved contractility. Cardiac enlargement is accompanied by...
全文获取路径: Elsevier  (合作)
影响因子:5.148 (2012)

  • hypertrophy 肥大
  • receptor 接受体
  • activated 激化了的
  • inhibition 抑制
  • signalling 发信号
  • concentric 同心状的
  • inhibitor 抑制剂
  • failure 破坏