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首页> 外文期刊>Archives of Toxicology >Sulfhydryl-mediated redox signaling in inflammation: role in neurodegenerative diseases
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Sulfhydryl-mediated redox signaling in inflammation: role in neurodegenerative diseases

机译：巯基介导的氧化还原信号在炎症中：在神经退行性疾病中的作用

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Posttranslational modifications of cysteine sulfhydryl (-SH) moieties, e.g., S-nitrosylation, S-glutathionylation, or S-sulfuration, play an important role in cellular response to oxidative stress. Reversible cysteine modifications alter protein function and can play a critical role in redox signal transduction. Perturbation of sulfhydryl homeostasis is a hallmark of many diseases, including neurodegenerative disorders. Besides direct oxidative stress within the neurons, inflammation of the central nervous system as well as the periphery is implicated also in the development and progression of neurodegeneration. Therefore, perturbation of redox regulation of key inflammatory mediators is an important component of neurodegenerative diseases. Many proteins involved in inflammation have been shown to undergo S-nitrosylation (-SNO) and/or S-glutathionylation (-SSG) with functional consequences. The mechanistic and functional relationships between these two modifications have yet to be thoroughly investigated. While protein-SNO intermediates in some cases may signal independently of protein-SSG intermediates, the relatively unstable nature of protein-SNO derivatives in the presence of GSH suggests that protein-SNO formation in many cases may serve as a precursor for protein-SSG modifications. In this review, we describe the cysteine modifications of specific inflammation-mediating proteins and their relationship to inflammatory responses such as cytokine and chemokine production. In particular, we consider evidence for sequential protein-SNO -> protein-SSG modifications of these proteins. We conclude that cysteine modifications of critical regulatory proteins are likely to play a central role in the onset and progression of neuroinflammatory diseases and thus should be studied thoroughly in this context.
机译：半胱氨酸巯基（-SH）部分的翻译后修饰，例如S-亚硝基化，S-谷胱甘肽酰化或S-硫化，在细胞对氧化应激的反应中起重要作用。可逆的半胱氨酸修饰会改变蛋白质功能，并在氧化还原信号转导中起关键作用。巯基稳态的摄动是许多疾病的标志，包括神经退行性疾病。除了神经元内的直接氧化应激外，中枢神经系统以及周围神经的炎症也与神经变性的发生和发展有关。因此，扰动关键炎症介质的氧化还原调节是神经退行性疾病的重要组成部分。已经显示出许多与炎症有关的蛋白质会发生S-亚硝基化（-SNO）和/或S-谷胱甘肽化（-SSG），并产生功能性后果。这两个修改之间的机械和功能关系尚待彻底研究。尽管蛋白质SNO中间体在某些情况下可能独立于蛋白质SSG中间体发出信号，但存在GSH的情况下蛋白质SNO衍生物的相对不稳定性质表明蛋白质SNO的形成在许多情况下可作为蛋白质SSG修饰的前体。在这篇综述中，我们描述了特定炎症介导蛋白的半胱氨酸修饰及其与炎症反应（如细胞因子和趋化因子产生）的关系。特别地，我们考虑了对这些蛋白质进行连续的蛋白质-SNO→蛋白质-SSG修饰的证据。我们得出结论，关键调节蛋白的半胱氨酸修饰可能在神经炎性疾病的发作和发展中起关键作用，因此应在此背景下进行深入研究。

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