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

NOX1/NADPH氧化酶在心律失常中作用的研究

• 批准号: 23659140
• 负责人: YABE Chihiro
• 金额: $ 2.41万
• 依托单位: Kyoto Prefectural University of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23659140/
• 关键词: 循環器・高血圧; 不整脈; チャネル; 活性酸素種

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.

活性氧（ROS）通过影响心肌细胞的离子通道而参与心房颤动的发病机制。在脓毒症动物模型中，心律失常的易感性增加。由于我们之前证明了一种新的超氧化物生成型 NADPH 氧化酶 NOX1 在脓毒症心脏中上调，从而引发心肌细胞凋亡，因此使用 Nox1 缺陷的小鼠研究了 NOX1 可能参与心律失常的发生。

项目成果

病態分子薬理学

病理分子药理学