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首页> 外文期刊>Journal of cellular physiology. >Apelin/APJ system: A novel promising target for neurodegenerative diseases
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Apelin/APJ system: A novel promising target for neurodegenerative diseases

机译：组织Apelin /已系统:承诺的目标神经退行性疾病

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摘要

Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD), are incurable diseases characterized by progressive loss of cognitive or motor function, which construct a serious threat to the life quality of aging populations and their life spans. Apelin is an endogenous ligand for the G protein-coupled receptor. Apelin is reported to be detected not only in the cardiovascular system but also in neurons of the central nervous system (CNS). In addition, alterations in the expression level of apelin appear to play a pivotal role in various physiological processes including loss of structure or function of neurons, inflammatory responses, oxidative stress, Ca~(2+) signaling, apoptosis, and autophagy. All of these processes are intimately related to the occurrence of neurodegenerative diseases. Recently, apelin is reported to improve cognitive impairment in PD by antioxidant and antiapoptotic properties. Hence, it is becoming increasingly appreciated that altering the level of apelin can change the course or dictate the outcome of neurodegenerative events such as AD, PD, and HD, suggesting that apelin could be a potential target for the treatment of neurodegenerative diseases possibly acting on a variety of signaling pathways such as suppression of inflammatory responses, inhibition of oxidative stress, reduction of Ca~(2+) signaling, induction of autophagy, and suppression of apoptosis.
机译：神经退行性疾病,包括阿尔茨海默氏症病(AD),帕金森病(PD)亨廷顿氏病(HD),是无法治愈的疾病特点是进步的认知或损失运动机能,构造一个严重的威胁人口老龄化和生活质量的他们的寿命。G protein-coupled受体。据报道,不仅被探测到的心血管系统也的神经元中枢神经系统(CNS)。改变组织apelin的表达水平似乎在各方面发挥关键作用生理过程包括损失结构或功能的神经元,炎症反应,氧化应激,Ca ~(2 +)信号,细胞凋亡和自噬。密切相关的发生吗神经退行性疾病。据报道,改善PD的认知障碍抗氧化和抗凋亡属性。越来越欣赏改变组织apelin可以改变的程度课程或决定的结果神经退行性活动,比如广告、PD和高清,这表明组织apelin可能是潜在的治疗神经退行性的目标可能作用于各种各样的疾病信号通路抑制等炎症反应,抑制氧化压力,减少Ca ~(2 +)信号,归纳自噬和凋亡的抑制。

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