Nitric Oxide: Exploring the Contextual Link with Alzheimer's Disease.

Nitric Oxide: Exploring the Contextual Link with Alzheimer's Disease.
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DOI:
10.1155/2016/7205747
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发表时间:
2016
影响因子:
--
通讯作者:
Jeong NY
Jeong NY
中科院分区:
生物学2区
文献类型:
--
作者:
Asiimwe N;Yeo SG;Kim MS;Jung J;Jeong NY

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神经元炎症是一个有系统组织的生理步骤,通常是为了抵抗入侵的病原体或清除体内受损和/或死亡的细胞碎片而触发的。这种炎症反应的关键是非神经元细胞的分布:小胶质细胞、星形胶质细胞和血源性巨噬细胞。神经胶质细胞分泌大量生物活性分子,包括促炎因子和一氧化氮(NO)。从免疫调节到神经调节,一氧化氮是一种著名的广泛生理系统的调节剂。它本质上是通过与环GMP (cGMP)相互作用介导这些生理效应,导致细胞内钙离子的调节。NO调节促炎分子的释放,与ROS相互作用导致活性氮物种(RNS)的形成,并靶向线粒体等重要细胞器,最终导致细胞死亡,这是许多神经退行性疾病的标志。AD是一种病因不明的衰弱性神经退行性疾病。由于积累的实验数据不断强调NO在神经炎症和AD进展中的作用,我们探索了最新的数据,以详细介绍新研究的NO在中枢神经系统神经元炎症和氧化应激相关神经退行性变中的相关分子机制,并为针对NO的治疗方法奠定了最新的知识。
Neuronal inflammation is a systematically organized physiological step often triggered to counteract an invading pathogen or to rid the body of damaged and/or dead cellular debris. At the crux of this inflammatory response is the deployment of nonneuronal cells: microglia, astrocytes, and blood-derived macrophages. Glial cells secrete a host of bioactive molecules, which include proinflammatory factors and nitric oxide (NO). From immunomodulation to neuromodulation, NO is a renowned modulator of vast physiological systems. It essentially mediates these physiological effects by interacting with cyclic GMP (cGMP) leading to the regulation of intracellular calcium ions. NO regulates the release of proinflammatory molecules, interacts with ROS leading to the formation of reactive nitrogen species (RNS), and targets vital organelles such as mitochondria, ultimately causing cellular death, a hallmark of many neurodegenerative diseases. AD is an enervating neurodegenerative disorder with an obscure etiology. Because of accumulating experimental data continually highlighting the role of NO in neuroinflammation and AD progression, we explore the most recent data to highlight in detail newly investigated molecular mechanisms in which NO becomes relevant in neuronal inflammation and oxidative stress-associated neurodegeneration in the CNS as well as lay down up-to-date knowledge regarding therapeutic approaches targeting NO.
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