NOX2调控钠电流在肥胖相关房颤发病中的分子机制

肥胖与房颤密切相关，作为独立危险因素对房颤发生的风险和预后有着重要影响，但具体机制不详。新近研究表明，钠电流极可能参与了肥胖诱发的房颤。我们前期研究和文献均显示，钠电流异常在房颤的发生和维持中起着关键作用。氧化应激特别是NOX2对肥胖的病理生理和房颤均有调控效应，该通路可直接调节钠电流。据此假设：NOX2对钠电流的调节，可能是肥胖相关房颤发生的关键。本研究拟应用多种技术，从不同层面明确肥胖对心房电重构和房颤发生的影响；探究NOX2对肥胖时心房细胞钠电流作用的具体机制；解释NOX2在肥胖所致心房电重构及房颤发生中的效应。试图从NOX2对钠电流调控的角度，解释肥胖相关房颤发生的机制。

Obesity, as an independent risk factor of atrial fibrillation (AF), is closely related to AF and has an important impact on the occurrence and prognosis of AF, but the specific mechanism is unknown. Some latest researches suggest that sodium current may be involved in obesity-induced AF and our previous studies as well as articles have demonstrated that the abnormal sodium current plays a key role in the pathogenesis and maintenance of AF. Oxidative stress, especially NOX2, which can directly regulate sodium current, has a regulatory effect on the pathophysiology of obesity and the occurrence of AF. Accordingly, we assume that the regulation of sodium current by NOX2 may be the key to the occurrence of obesity-related AF. Therefore, in this study, a variety of techniques will be used to clarify the effect of obesity on atrial electrical remodeling and AF from different levels, to explore the specific mechanism of function of NOX2 on the sodium current in atrial myocytes in obesity, and to explain the influence of NOX2 on the occurrence of obesity-induced atrial electrical remodeling and AF. The aim of this study is to elucidate the mechanism of obesity-related AF from the perspective of NOX2 regulating sodium current.