摘要
一氧化氮在神经退行性疾病的发病机制和进展中的作用如帕金森氏症和阿尔茨海默氏病在过去几年中已变得很突出。产生活性氧的酶的活性增加,降低抗氧化酶活性和谷胱甘肽池的不平衡调解和标记的神经退行性过程。许多蛋白质的氧化损伤是由一氧化氮合成酶(NOS)在一氧化氮的生产过剩后带来和随后的反应与活性氧。蛋白质组学的方法已经非常领先,通过促进定量评估的差异表达模式和氧化修饰的蛋白质和边沿,映射它们的非规范功能。作为一个信号分子参与多个生化途径,一氧化氮水平受到严格的规定。所有三种一氧化氮合成酶亚型在阿尔茨海默病中的表达显示异常模式,改变了细胞内的信号转导和简单的氧化应激路由方向。本综述讨论在发展的神经退行性疾病中控制一氧化氮的生物合成的主要因素,后续反应以及随后的影响。
关键词: 阿尔茨海默病,蛋白质相互作用,金属平衡,神经退行性疾病,一氧化氮,一氧化氮合酶,氧化应激,蛋白质组学。
Current Alzheimer Research
Title:Nitric Oxide Homeostasis in Neurodegenerative Diseases
Volume: 13 Issue: 2
Author(s): Luciana Hannibal
Affiliation:
关键词: 阿尔茨海默病,蛋白质相互作用,金属平衡,神经退行性疾病,一氧化氮,一氧化氮合酶,氧化应激,蛋白质组学。
摘要: The role of nitric oxide in the pathogenesis and progression of neurodegenerative illnesses such as Parkinson’s and Alzheimer’s diseases has become prominent over the years. Increased activity of the enzymes that produce reactive oxygen species, decreased activity of antioxidant enzymes and imbalances in glutathione pools mediate and mark the neurodegenerative process. Much of the oxidative damage of proteins is brought about by the overproduction of nitric oxide by nitric oxide synthases (NOS) and its subsequent reactivity with reactive oxygen species. Proteomic methods have advanced the field tremendously, by facilitating the quantitative assessment of differential expression patterns and oxidative modifications of proteins and alongside, mapping their non-canonical functions. As a signaling molecule involved in multiple biochemical pathways, the level of nitric oxide is subject to tight regulation. All three NOS isoforms display aberrant patterns of expression in Alzheimer’s disease, altering intracellular signaling and routing oxidative stress in directions that are uncompounded. This review discusses the prime factors that control nitric oxide biosynthesis, reactivity footprints and ensuing effects in the development of neurodegenerative diseases.
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Cite this article as:
Luciana Hannibal , Nitric Oxide Homeostasis in Neurodegenerative Diseases, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205012666150921101250
DOI https://dx.doi.org/10.2174/1567205012666150921101250 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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