Established Principles and Emerging Concepts on the Interplay between Mitochondrial Physiology and S-(De)nitrosylation: Implications in Cancer and Neurodegeneration.

Established Principles and Emerging Concepts on the Interplay between Mitochondrial Physiology and S-(De)nitrosylation: Implications in Cancer and Neurodegeneration.
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DOI:
10.1155/2012/361872
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发表时间:
2012
影响因子:
--
通讯作者:
Filomeni G
Filomeni G
中科院分区:
其他
文献类型:
--
作者:
Di Giacomo G;Rizza S;Montagna C;Filomeni G

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S-亚硝基化是半胱氨酸残基的翻译后修饰,其经常被指示为在一氧化氮(过量)产生下游的氧化还原不平衡时控制细胞响应的潜在分子机制。在过去的几年中,S-亚硝基硫醇(SNO)水平的增加与基于氮氧化应激的病理学的发作(例如,癌症和神经变性),其中线粒体稳态的改变和依赖于它的细胞过程的激活的病症也已被报道。在本文中,我们的目的是总结目前的知识,进行S-亚硝基化,这种氧化还原修饰可能会影响线粒体功能,其损害已与肿瘤发生和神经细胞死亡的相关蛋白质。特别是,重点将给予可能的,但仍然被忽视的影响,脱亚硝基化反应在线粒体SNO的调制,以及它们如何影响线粒体相关的细胞过程,如氧化磷酸化,线粒体动力学和线粒体自噬。
S-nitrosylation is a posttranslational modification of cysteine residues that has been frequently indicated as potential molecular mechanism governing cell response upon redox unbalance downstream of nitric oxide (over)production. In the last years, increased levels of S-nitrosothiols (SNOs) have been tightly associated with the onset of nitroxidative stress-based pathologies (e.g., cancer and neurodegeneration), conditions in which alterations of mitochondrial homeostasis and activation of cellular processes dependent on it have been reported as well. In this paper we aim at summarizing the current knowledge of mitochondria-related proteins undergoing S-nitrosylation and how this redox modification might impact on mitochondrial functions, whose impairment has been correlated to tumorigenesis and neuronal cell death. In particular, emphasis will be given to the possible, but still neglected implication of denitrosylation reactions in the modulation of mitochondrial SNOs and how they can affect mitochondrion-related cellular process, such as oxidative phosphorylation, mitochondrial dynamics, and mitophagy.