Department of Biochemistry, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong.
Apoptosis. 2010 Nov;15(11):1364-70. doi: 10.1007/s10495-010-0464-1.
Nitric oxide (NO) is a gaseous signaling molecule in the biological system. It mediates its function through the direct modification of various cellular targets, such as through S-nitrosylation. The process of S-nitrosylation involves the attachment of NO to the cysteine residues of proteins. Interestingly, an increasing number of cellular pathways are found to be regulated by S-nitrosylation, and it has been proposed that this redox signaling pathway is comparable to phosphorylation in cells. However, imbalance of NO metabolism has also been linked to a number of human diseases. For instance, NO is known to contribute to neurodegeneration by causing protein nitration, lipid peroxidation and DNA damage. Moreover, recent studies show that NO can also contribute to the process of neurodegeneration through the impairment of pro-survival proteins by S-nitrosylation. Thus, further understanding of how NO, through S-nitrosylation, can compromise neuronal survival will provide potential therapeutic targets for neurodegenerative diseases.
一氧化氮（NO）是生物系统中的一种气态信号分子。它通过直接修饰各种细胞靶标来发挥其功能，例如通过 S-亚硝基化。S-亚硝基化的过程涉及将 NO 附着到蛋白质的半胱氨酸残基上。有趣的是，越来越多的细胞途径被发现受到 S-亚硝基化的调节，有人提出这种氧化还原信号通路与细胞中的磷酸化相当。然而，NO 代谢的失衡也与许多人类疾病有关。例如，NO 通过引起蛋白质硝化、脂质过氧化和 DNA 损伤，导致神经退行性变。此外，最近的研究表明，NO 还可以通过 S-亚硝基化损害抗凋亡蛋白来促进神经退行性变的发生。因此，进一步了解 NO 通过 S-亚硝基化如何损害神经元的存活，将为神经退行性疾病提供潜在的治疗靶点。
