CAJ | 학술논문

氧化应激引起的心脏收缩功能障碍和心律失常均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外；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，导致心律失常发生。
양화응격인기적심장수축공능장애화심률실상균원우세포내외납개리자은태실형，기잠재적세포내신호조공궤제제료경전도경，여통과조공단백격매A、단백격매C화개리자/개조소의뢰성단백격매Ⅱ등단백격매사지활화외；근래유래유다적증거현시양화응격시활성양자유기야능구직접양화저사격매혹자납개리자전운단백화리자통도，종이개변기작용，도치심률실상발생。
Cardiac contractile dysfunction and arrhythmic genesis are resulted from disturbed intracellular Na+and Ca2+ handling under condition of oxidation stress. Stress-induced intracellular signaling regulated mechanisms in which many activated stress kinases, such as cAMP-dependent protein kinase A, protein kinase C , Ca/calmodulin-dependent pro-tein kinaseⅡand classical pathways, are known to be involved. However, it is becoming increasingly evident that reactive oxygen species may directly oxidize these kinases, Na+and Ca2+channel protein and transporters, which lead to changing of intracellular Na+and Ca2+accumulation, and to trigger of arrhythmias.