JAK/STAT信号转导通路与心力衰竭的研究进展

Progress of JAK/STAT Signal Transduction Pathway and Heart Failure

对于心力衰竭的研究,已由20世纪80年代后期主张神经体液过度激活改变血流动力学加剧心室重构是心力衰竭重要的病理生理机制,转变为当今细胞分子的研究,白介素激活的Janus激酶(JAK)/信号转导及转录激活因子(signal transduction and activator of transcription,STAT)也可介导心肌缺血再灌注损伤、心肌肥大、心室重构、心肌炎症等,甚至可影响局部肾素-血管紧张素-醛固酮系统,因其影响了心力衰竭过程中的各个环节,目前已成为国际心力衰竭领域研究的热点,现着重从JAK/STAT信号转导通路的结构、激活途径、介导心力衰竭的机制几个方面对JAK/STAT信号转导通路在心力衰竭中的研究进展做一综述,并阐述干预JAK/STAT信号转导通路从而干预心力衰竭的研究进展。

For study of heart failure,it has been changed from excessive activation of neurohumor and hemodynamics in late 1980s to ventricular remodeling. Cell molecule has become a new direction to study heart failure. Interleukin activation of Janus kinase （JAK） /signal transducer and activator of transcription （STAT） can also be mediated by myocardial ischemia reperfusion injury, myocardial hypertrophy and ventricular remodeling,inflammation,and even affect the renin-angiotensin-aldosterone system. We focused on the study of JAK/STAT be-cause of its influence on all aspects of heart failure. This paper focused on several aspects of structure and activation pathway of JAK/STAT signaling pathway,and the mechanism of mediating heart failure. It reviews the research progress of intervening JAK/STAT signaling path-way, and thus intervening heart failure.