首页> 美国卫生研究院文献>International Journal of Molecular Sciences >The Roles of Nitric Oxide Synthase/Nitric Oxide Pathway in the Pathology of Vascular Dementia and Related Therapeutic Approaches
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The Roles of Nitric Oxide Synthase/Nitric Oxide Pathway in the Pathology of Vascular Dementia and Related Therapeutic Approaches

机译:一氧化氮合酶/一氧化氮通路在血管痴呆病理学中的作用及相关治疗方法

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摘要

Vascular dementia (VaD) is the second most common form of dementia worldwide. It is caused by cerebrovascular disease, and patients often show severe impairments of advanced cognitive abilities. Nitric oxide synthase (NOS) and nitric oxide (NO) play vital roles in the pathogenesis of VaD. The functions of NO are determined by its concentration and bioavailability, which are regulated by NOS activity. The activities of different NOS subtypes in the brain are partitioned. Pathologically, endothelial NOS is inactivated, which causes insufficient NO production and aggravates oxidative stress before inducing cerebrovascular endothelial dysfunction, while neuronal NOS is overactive and can produce excessive NO to cause neurotoxicity. Meanwhile, inflammation stimulates the massive expression of inducible NOS, which also produces excessive NO and then induces neuroinflammation. The vicious circle of these kinds of damage having impacts on each other finally leads to VaD. This review summarizes the roles of the NOS/NO pathway in the pathology of VaD and also proposes some potential therapeutic methods that target this pathway in the hope of inspiring novel ideas for VaD therapeutic approaches.
机译:血管痴呆(VAD)是全球痴呆症的第二种最常见的形式。它是由脑血管疾病引起的,患者往往表现出对先进的认知能力的严重损害。一氧化氮合酶(NOS)和一氧化氮(NO)在VAD的发病机制中起重要作用。 NO的功能由其浓度和生物利用度决定,其由NOS活性调节。大脑中不同NOS亚型的活动是分区的。病理上,内皮NOS被灭活,这导致不充分的生产,并且在诱导脑血管内皮功能障碍之前加重氧化应激,而神经元NOS过度活跃并且可以产生过量的否导致神经毒性。同时,炎症刺激诱导型NoS的巨大表达,这也产生过量的NO,然后诱导神经炎症。这些伤害的恶性循环彼此影响最终导致VAD。本综述总结了NOS / NO途径在VAD病理学中的作用,并提出了一些潜在的治疗方法,以希望激发VAD治疗方法的新颖思想希望。

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