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长链非编码RNA NEAT1:神经退行性疾病的关键因素。

lncRNA NEAT1: Key player in neurodegenerative diseases.

作者信息

Li Kun, Wang Ziqiang

机构信息

Department of Nuclear Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan 250014, China.

Department of Nuclear Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan 250014, China; Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250062, China.

出版信息

Ageing Res Rev. 2023 Apr;86:101878. doi: 10.1016/j.arr.2023.101878. Epub 2023 Feb 3.

Abstract

Neurodegenerative diseases are the most common causes of disability worldwide. Given their high prevalence, devastating symptoms, and lack of definitive diagnostic tests, there is an urgent need to identify potential biomarkers and new therapeutic targets. Long non-coding RNAs (lncRNAs) have recently emerged as powerful regulatory molecules in neurodegenerative diseases. Among them, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be upregulated in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). However, whether this is part of a protective or harmful mechanism is still unclear. This review summarizes our current knowledge of the role of NEAT1 in neurodegenerative diseases and its association with the characteristic aggregation of misfolded proteins: amyloid-β and tau in AD, α-synuclein in PD, mutant huntingtin in HD, and TAR DNA-binding protein-43 fused in sarcoma/translocated in liposarcoma in ALS. The aim of this review is to stimulate further research on more precise and effective treatments for neurodegenerative diseases.

摘要

神经退行性疾病是全球致残的最常见原因。鉴于其高患病率、严重症状以及缺乏明确的诊断测试,迫切需要识别潜在的生物标志物和新的治疗靶点。长链非编码RNA(lncRNA)最近已成为神经退行性疾病中强大的调控分子。其中,lncRNA核副斑点组装转录本1(NEAT1)已被报道在阿尔茨海默病(AD)、帕金森病(PD)、亨廷顿舞蹈病(HD)和肌萎缩侧索硬化症(ALS)中上调。然而,这是保护机制还是有害机制的一部分仍不清楚。本综述总结了我们目前对NEAT1在神经退行性疾病中的作用及其与错误折叠蛋白特征性聚集的关联的认识:AD中的淀粉样β蛋白和tau蛋白、PD中的α-突触核蛋白、HD中的突变亨廷顿蛋白以及ALS中的肉瘤融合/脂肪肉瘤易位的TAR DNA结合蛋白43。本综述的目的是激发对神经退行性疾病更精确有效治疗方法的进一步研究。

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