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心脏氧化还原系统对钠钙处理蛋白的调控机制

刘衍恭,刘刚,王普,郑明奇   

  1. 河北医科大学第一医院
  • 收稿日期:2014-04-24 修回日期:2014-06-17 出版日期:2014-10-15 发布日期:2014-10-15
  • 通讯作者: 郑明奇

Redox regulation of cardiac Na and Ca handling protein

LIU Yan gong1,LIU Gang 1,WANG Pu 1,ZHENG Ming qi2   

  1. 1. Department of Cardiology, the 1st Hospital of Hebei Medical University, Shijiazhuang 050031, China
    2.
  • Received:2014-04-24 Revised:2014-06-17 Published:2014-10-15 Online:2014-10-15
  • Contact: ZHENG Ming qi

摘要: 氧化应激引起的心脏收缩功能障碍和心律失常都源于细胞内外钠钙离子稳态失衡。其潜在的细胞内信号调控机制除了经典途径,如通过调控蛋白激酶A、蛋白激酶C和钙离子/钙调素依赖性蛋白激酶Ⅱ等蛋白激酶使之活化;近来愈来愈多的证据显示氧化应激时活性氧自由基也能够直接氧化这些激酶或者钠钙离子转运蛋白和离子通道,从而改变其作用,促进心律失常发生。

关键词: 氧化应激, 钠钙处理, 活性氧自由基, 氧化还原系统, 心律失常

Abstract: Abstract: Cardiac contractile dysfunction and arrhythmic genesis result from disturbed intracellular Na+ and Ca2+ handling in condition of oxidation stress. Stress-induced intracellular signaling regulation mechanisms in which many activated stress kinases, such cAMP-dependent protein kinase A, protein kinase C and Ca/calmodulin-dependent protein kinase Ⅱ as classical pathways, are known involved. However, it is becoming increasingly evidence that reactive oxygen species may directly oxidize these kinases, Na+ and Ca2+ channel protein and transports, leading to alter the intracellular Na+ and Ca2+ accumulation, to trigger arrhythmias.

Key words: Oxidation stress, reactive oxygen species, Na+ and Ca2+ handling, redox system, arrhythmias