中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2024, Vol. 20 ›› Issue (2): 402-415.doi: 10.4103/NRR.NRR-D-23-01353

• 综述:退行性病与再生 • 上一篇    下一篇

一氧化氮在血管性痴呆突触功能障碍中的新作用

  

  • 出版日期:2025-02-15 发布日期:2024-06-18
  • 基金资助:
    国家重点研发计划项目；国家自然科学基金；2014年中国青年拔尖人才计划；华中科技大学学术前沿青年团队；湖北省自然科学基金项目；湖南省科技创新计划项目；湖南省自然科学基金项目；国家自然科学基金面上项目；江西省教育厅科技项目；江西省自然科学基金项目；江西省认知科学与交叉学科研究中心研究项目

The emerging role of nitric oxide in the synaptic dysfunction of vascular dementia

Xiaorong Zhang1, 2, 3, #, Zhiying Chen2, 4, #, Yinyi Xiong2, 5, Qin Zhou2 , Ling-Qiang Zhu6, *, Dan Liu6, *   

  1. 1 Department of Pathology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi Province, China; 2 Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi Province, China; 3 Center for Cognitive Science and Transdisciplinary Studies, Jiujiang University, Jiangxi Province, China; 4 Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi Province, China; 5 Department of Rehabilitation, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi Province, China; 6 Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
  • Online:2025-02-15 Published:2024-06-18
  • Contact: Ling-Qiang Zhu, MD, zhulq@mail.hust.edu.cn; Dan Liu, MD, liudan_echo@mail.hust.edu.cn.
  • Supported by:
    This work was supported by the National Key R & D Program of China, No. 2019YFE0121200 (to LQZ); the National Natural Science Foundation of China, Nos. 82325017 (to LQZ), 82030032 (to LQZ), 82261138555 (to DL); the Natural Science Foundation of Hubei Province, No. 2022CFA004 (to LQZ); the Natural Science Foundation of Jiangxi Province, No. 20224BAB206040 (to XZ); and Research Project of Cognitive Science and Transdisciplinary Studies Center of Jiangxi Province, No. RZYB202201 (to XZ).

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摘要：

一氧化氮是一种普遍存在的气体细胞信使，参与中枢神经系统的多种生理和病理过程。在血管性痴呆中不同阶段，一氧化氮的含量及生物利用度是不断变化的，在晚期出现显著下降，影响血管性痴呆的认知功能障碍。一氧化氮是一把双刃剑，生理浓度的一氧化氮具有神经保护作用，但一氧化氮的缺乏或过量都可能导致突触功能障碍及神经元的损伤；然而，在血管性痴呆中的作用机制尚不完全清楚。文章首先总结了最近一氧化氮在生理状态下和血管性痴呆病理状态下的变化情况。然后，重点讨论了一氧化氮对血管性痴呆中突触功能障碍的影响及其作用机制，包括突触前及突触后功能障碍、神经炎症、氧化应激、血脑屏障功能障碍、内质网应激等方面对血管性痴呆发展的作用机制。此外，靶向NO-sGC-cGMP通路，提高一氧化氮含量及生物利用度可能为血管性痴呆提供了一种新的治疗策略。

https://orcid.org/0000-0001-9964-9229 (Ling-Qiang Zhu); https://orcid.org/0000-0001-8078-4674 (Dan Liu)

Abstract: With an increase in global aging, the number of people affected by cerebrovascular diseases is also increasing, and the incidence of vascular dementia—closely related to cerebrovascular risk—is increasing at an epidemic rate. However, few therapeutic options exist that can markedly improve the cognitive impairment and prognosis of vascular dementia patients. Similarly in Alzheimer’s disease and other neurological disorders, synaptic dysfunction is recognized as the main reason for cognitive decline. Nitric oxide is one of the ubiquitous gaseous cellular messengers involved in multiple physiological and pathological processes of the central nervous system. Recently, nitric oxide has been implicated in regulating synaptic plasticity and plays an important role in the pathogenesis of vascular dementia. This review introduces in detail the emerging role of nitric oxide in physiological and pathological states of vascular dementia and summarizes the diverse effects of nitric oxide on different aspects of synaptic dysfunction, neuroinflammation, oxidative stress, and blood–brain barrier dysfunction that underlie the progress of vascular dementia. Additionally, we propose that targeting the nitric oxide-sGC-cGMP pathway using certain specific approaches may provide a novel therapeutic strategy for vascular dementia.

Key words: endoplasmic reticulum stress, endothelial nitric oxide synthase, gene therapy, nitric oxide, NO-sGC-cGMP pathway, synaptic dysfunction, vascular dementia