神经生长因子介导神经节丛亢进与心房颤动的循环

LiDong Cai, Shao-wen Liu
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引用次数: 1

摘要

神经节神经丛(Ganglionated Plexus, GP)是由心脏内在自主神经系统(ANS)组成的复杂神经网络,主要分布在肺静脉(pv)上腔周围的脂肪垫中。近期研究表明,心脏全科医生亢进与房颤形成恶性循环,心脏全科医生亢进促进房颤的发生和维持,随着房颤的持续,心脏全科医生亢进增加。此外,研究证实Nav1.8通道在GPs中高表达,与GPs的活性和AF的诱导密切相关。神经生长因子(NGF)是一种重要的神经营养因子,AF时,NGF在GPs中的表达随着时间的推移而上调,可通过TRPV1信号通路触发SP在心脏的释放。此外,SP能快速增加Nav1.8通道的活性,表现为感觉神经动作电位的增加。因此,我们假设房颤期间NGF的上调可以通过TRPV1-SP-Nav1.8通道通路增加gp的活性,有助于房颤的稳定性。如果这一假设被证明是正确的,未来基于这一联系的研究可能有助于寻找房颤治疗的新靶点。
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Nerve Growth Factor Mediates the Vious Cycle between Hyperactivity ofGanglionated Plexus and Atrial Fibrillation
Ganglionated Plexus (GP) is a complex neural network composed by intrinsic cardiac autonomic nervous system (ANS) and is mainly located in fat pads around the antrum of the pulmonary veins (PVs). Recent studies demonstrated hyperactivity of GPs and atrial fibrillation (AF) formed a vicious cycle, to be specific, hyperactivity of the cardiac GPs facilitated the initiation and maintenance of AF and the activity of cardiac GPs increased as AF continued. In addition, research has confirmed that the Nav1.8 channel is highly expressed in GPs and is closely related to activity of GPs and the inducibility of AF. Nerve growth factor (NGF) is an important neurotrophic factor and the expression of NGF in GPs is up-regulated during AF over time, which could trigger the release of SP in the heart via TRPV1 signaling pathways. Besides, SP could rapidly increase the activity of the Nav1.8 channel, demonstrating the increment of Sensory nerve action potentials. Therefore, we hypothesized that up-regulated NGF during AF could increase the activity of GPs through TRPV1-SP-Nav1.8 channel pathways and contributes to stability of AF. If this hypothesis is proved to be correct, future studies based on this link may help to find new therapeutic targets for the treatment of AF.
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