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一氧化氮介导的S-亚硝基化作用在人类生理和病理状态下的信号转导中发挥作用(综述)。

Nitric oxide‑mediated S‑Nitrosylation contributes to signaling transduction in human physiological and pathological status (Review).

作者信息

Xu Yan, Wang Xuesong, Zhou Xiaolei, Peng Lulu, Yuan Jiayi, Zhang Yichi, Wu Nan, Ye Junsong

机构信息

Subcenter for Stem Cell Clinical Translation, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China.

First Clinical College of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China.

出版信息

Int J Mol Med. 2025 Oct;56(4). doi: 10.3892/ijmm.2025.5593. Epub 2025 Jul 25.

DOI:10.3892/ijmm.2025.5593
PMID:40709391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12306599/
Abstract

In the complex development of various diseases, nitric oxide‑mediated S‑nitrosylation is increasingly recognized for its distinct regulatory function. Recent research has advanced our knowledge of how this nitric oxide‑dependent modification is dynamically controlled under both physiological and pathological conditions. S‑nitrosylation plays a key role in regulating mitochondrial function, gene transcription, cellular homeostasis and metabolism and it is also involved in the pathogenesis of cardiovascular disorders, neurological conditions and cancer. The present review outlined the signaling pathways driven by nitric oxide and describes the formation, specificity and factors that influence S‑nitrosylation levels. It also compared the strengths and limitations of different detection methods for S‑nitrosation reactions. The present review discussed the cellular regulatory mechanisms affected by S‑nitrosylation to clarify how certain major diseases are connected to specific S‑nitrosylated proteins. These insights may guide the development of targeted repair strategies for malfunctioning proteins by focusing on defined S‑nitrosylation sites, offering theoretical support for disease intervention and treatment.

摘要

在各种疾病的复杂发展过程中,一氧化氮介导的S-亚硝基化因其独特的调节功能而越来越受到认可。最近的研究增进了我们对这种依赖一氧化氮的修饰在生理和病理条件下如何动态调控的认识。S-亚硝基化在调节线粒体功能、基因转录、细胞内稳态和代谢中起关键作用,并且还参与心血管疾病、神经疾病和癌症的发病机制。本综述概述了由一氧化氮驱动的信号通路,描述了S-亚硝基化的形成、特异性以及影响其水平的因素。它还比较了不同的S-亚硝基化反应检测方法的优缺点。本综述讨论了受S-亚硝基化影响的细胞调节机制,以阐明某些主要疾病如何与特定的S-亚硝基化蛋白相关联。这些见解可能通过聚焦于特定的S-亚硝基化位点来指导针对功能失调蛋白的靶向修复策略的开发,为疾病干预和治疗提供理论支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/aec081469eae/ijmm-56-04-05593-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/6a3ee2678fda/ijmm-56-04-05593-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/13bab23847f3/ijmm-56-04-05593-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/9591b0596050/ijmm-56-04-05593-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/aec081469eae/ijmm-56-04-05593-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/6a3ee2678fda/ijmm-56-04-05593-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/13bab23847f3/ijmm-56-04-05593-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/9591b0596050/ijmm-56-04-05593-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ccb/12306599/aec081469eae/ijmm-56-04-05593-g03.jpg

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本文引用的文献

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A Fluorescent Probe for Imaging and Treating S-Nitrosation Stress in OGD/R Cells.一种用于成像和治疗氧糖剥夺/复氧(OGD/R)细胞中S-亚硝基化应激的荧光探针。
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The evolution of S-nitrosylation detection methodology and the role of protein S-nitrosylation in various cancers.S-亚硝基化检测方法的演变以及蛋白质S-亚硝基化在各种癌症中的作用。
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Aging Dis. 2024 Mar 25;16(5):2641-2658. doi: 10.14336/AD.2024.0099.
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S-Nitrosylation of Septin2 Exacerbates Aortic Aneurysm and Dissection by Coupling the TIAM1-RAC1 Axis in Macrophages.S-亚硝基化修饰的Septin2 通过偶联巨噬细胞中的 TIAM1-RAC1 轴加剧了主动脉瘤和夹层。
Circulation. 2024 Jun 11;149(24):1903-1920. doi: 10.1161/CIRCULATIONAHA.123.066404. Epub 2024 Feb 15.
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Nitric Oxide: Physiological Functions, Delivery, and Biomedical Applications.一氧化氮:生理功能、传递和生物医学应用。
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Mitochondrial GSNOR Alleviates Cardiac Dysfunction via ANT1 Denitrosylation.线粒体 GSNOR 通过 ANT1 脱硝基化缓解心脏功能障碍。
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FAT-switch-based quantitative S-nitrosoproteomics reveals a key role of GSNOR1 in regulating ER functions.基于 FAT 开关的定量 S-亚硝基蛋白质组学揭示了 GSNOR1 在调节内质网功能中的关键作用。
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Cathepsin B S-nitrosylation promotes ADAR1-mediated editing of its own mRNA transcript via an ADD1/MATR3 regulatory axis.组织蛋白酶 B 的 S-亚硝基化通过 ADD1/MATR3 调节轴促进 ADAR1 介导的自身 mRNA 转录本的编辑。
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