摘要
背景:一氧化氮(NO)介导的细胞信号传递是一种多方面的机制,调节着不同组织中的代谢活动和命运。过亚硝酸根(ONOO-)是一氧化氮自由基和超氧物的反应产物,与细胞膜、磷脂和蛋白质相互作用,造成损伤。目的:蛋白质分子在翻译后修饰和脂质硝化过程中生成硝基酪氨酸(ONOO-酪氨酸)和(或)硝基半胱氨酸(ONOO-半胱氨酸)的反应动力学是决定细胞存活或凋亡信号机制的关键。结果:亚硝基化对鸟苷酸环化酶的活化和GPCRs有调节作用,并能调节NF-κB的活化。最近的研究结果显示了S-亚硝基化的神经保护作用,但其作用机制尚不清楚.结论:在考虑背景的同时,我们还讨论了NO衍生物在医学中的生物学作用。我们针对四个已知的化合物:Snap,sin-1氯化物,SNP和GSNO来了解NO在不同组织中的作用。在这里,我们分析现有的发现,以评估NO信号在炎症,血管扩张和耐受性治疗的相关性。
关键词: 一氧化氮,亚硝基化,G蛋白偶联受体,炎症,神经变性。
图形摘要
Current Drug Targets
Title:S-Nitrosylation in Regulation of Inflammation and Cell Damage
Volume: 19 Issue: 15
关键词: 一氧化氮,亚硝基化,G蛋白偶联受体,炎症,神经变性。
摘要: Background: Cell signaling through nitric oxide (NO) is a multifaceted mechanism, which regulates metabolic activities and fate in different tissues. The peroxynitrite (ONOO-) formed as reaction product of nitric oxide radical and superoxide interacts with cell membrane phospholipids and proteins causing damage.
Objective: The reaction kinetics to form nitrotyrosine (ONOO-tyrosine) and/or nitrosylated cysteine (ONOO-cysteine) in protein molecules during posttranslational modification and nitration of lipids are therefore critical in determining cells’ signaling mechanism for survival or apoptosis.
Results: The nitrosylation was found to modulate GPCRs and activation of guanylate cyclase as well as regulate NF-κB activation. The recent findings have shown the neuroprotective effects of S- nitrosylation, though mechanism is unclear.
Conclusion: While keeping the background in mind, we address here the biological function of NO derivatives in medicine. We target four known compounds: SNAP, SIN- 1 chloride, SNP and GSNO to understand the effect of NO in different tissues. Here we analyze the existing findings to assess therapeutic relevance of NO-signaling during inflammation, vasodilation and tolerance.
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Cite this article as:
S-Nitrosylation in Regulation of Inflammation and Cell Damage, Current Drug Targets 2018; 19 (15) . https://dx.doi.org/10.2174/1389450119666180213094747
DOI https://dx.doi.org/10.2174/1389450119666180213094747 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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