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

活性氧（ROS）通过影响心肌细胞的离子通道参与房颤的发病机制。在脓毒症动物模型中，对心律失常的易感性增强。由于我们之前证明了一种新型的产生超氧化物的NADPH氧化酶，NOX1，在败血症心脏中被上调以引起心肌细胞凋亡，因此我们使用NOX1缺乏的小鼠来研究NOX1在心律失常发展中的可能参与。

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.