A study on the role of NOX1/NADPH oxidase in cardiac arrhythmia

活性氧通过影响心肌细胞离子通道参与心房颤动的发病机制。在脓毒症动物模型中，对心律失常的易感性增加。由于我们以前证明，一种新的异构体的超氧化物生成NADPH氧化酶，NOX 1，在脓毒症心脏上调，引起心肌细胞凋亡，可能参与的NOX 1在心脏心律失常的发展进行了研究，使用小鼠缺乏NOX 1。

Reactive oxygen species (ROS) have been implicated in the pathogenesis of atrial fibrillation by affecting ion channels of cardiomyocytes. In animal model of sepsis, susceptibility to cardiac arrhythmia is augmented. Since we previously demonstrated that a novel isoform of superoxide-generating NADPH oxidase, NOX1, was up-regulated in septic heart to elicit cardiomyocyte apoptosis, a possible involvement of NOX1 in the development of cardiac arrhythmia was investigated using mice deficient in Nox1.