基础医学与临床 ›› 2014, Vol. 34 ›› Issue (8): 1129-1132.

• 短篇综述 • 上一篇    下一篇

心肌兴奋-收缩耦联在心力衰竭中的研究进展

李青,李菊香   

  1. 南昌大学第二附属医院
  • 收稿日期:2013-11-05 修回日期:2014-01-14 出版日期:2014-08-05 发布日期:2014-07-15
  • 通讯作者: 李菊香 E-mail:ljx912@126.com
  • 基金资助:
    国家自然科学基金(地区基金);江西省自然科学基金

Progress on Excitation–Contraction Coupling in Heart Failure

  • Received:2013-11-05 Revised:2014-01-14 Online:2014-08-05 Published:2014-07-15

摘要: 心肌兴奋-收缩耦联(ECC)是心脏电活动转换成机械收缩的过程,Ca2+释放通道(RyR2)在ECC中起核心作用。Ca2+和Na+转运参与ECC的全过程。Ca2+转运蛋白和细胞内激酶与心力衰竭的发生发展密切相关,Ca2+转运的改变常发生在心功能衰竭之前。Ca2+转运与Na+转运相互影响,细胞内Na+转运因细胞内Na+浓度和晚钠电流增加而受到干扰,舒张期Ca2+持续增加导致舒张功能障碍、并诱导心律失常。

关键词: 兴奋-收缩耦联, 钙/钙调蛋白依赖性蛋白激酶, 钙转运, 钠转运

Abstract: Excitation–contraction coupling is the process by which the cardiomyocyte translates electrical excitation into mechanical contraction. The RyR2 plays a central role in the process. Ca2+-handling and Na+-handling participate the whole process of excitation–contraction coupling. Alterations in Ca2+-handling proteins and intracellular kinases are involved in the pathogenesis of heart failure. Changes in Ca2+-handling often precede the depression of myocardial function. Intracellular Ca2+-handling is closely coupled with intracellular Na+-handling. Intracellular Na+-handling is disturbed with elevated intracellular Na+-concentration and increased late INa. Diastolic Ca2+ can consecutively increase contributing to diastolic dysfunction and heart failure as well as arrhythmias.

Key words: excitation–contraction coupling, calcium/calmodulin-dependent protein kinase II, Ca2+-handling, Na+-handling