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调控非编码 RNA 与氧化应激和神经炎症:帕金森病中的有趣串扰

Regulatory Non-coding RNAs Involved in Oxidative Stress and Neuroinflammation: An Intriguing Crosstalk in Parkinson's Disease.

机构信息

Department of Biology, Payam Noor University International, Center of Gheshm, Hormozgan, Iran.

Student Research Committee, Arak University of Medical Science, Arak, Iran.

出版信息

Curr Med Chem. 2024;31(34):5576-5597. doi: 10.2174/0929867331666230817102135.

DOI:10.2174/0929867331666230817102135
PMID:37592769
Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the accumulation of α-synuclein and the degeneration of dopaminergic neurons in the substantia nigra. Although the molecular bases for PD development are not fully recognized, extensive evidence has suggested that the development of PD is strongly associated with neuroinflammation. It is noteworthy that while neuroinflammation might not be a primary factor in all patients with PD, it seems to be a driving force for disease progression, and therefore, exploring the role of pathways involved in neuroinflammation is of great importance. Besides, the importance of non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and competing endogenous RNAs (ceRNAs), has been widely studied with a focus on the pathogenesis of PD. However, there is no comprehensive review regarding the role of neuroinflammation- related ncRNAs as prospective biomarkers and therapeutic targets involved in the pathogenesis of PD, even though the number of studies connecting ncRNAs to neuroinflammatory pathways and oxidative stress has markedly increased in the last few years. Hence, the present narrative review intended to describe the crosstalk between regulatory ncRNAs and neuroinflammatory targets with respect to PD to find and propose novel combining biomarkers or therapeutic targets in clinical settings.

摘要

帕金森病(PD)是一种常见的神经退行性疾病,其特征是α-突触核蛋白的积累和黑质中多巴胺能神经元的退化。尽管 PD 发展的分子基础尚未完全被认识,但大量证据表明 PD 的发展与神经炎症密切相关。值得注意的是,虽然神经炎症可能不是所有 PD 患者的主要因素,但它似乎是疾病进展的驱动力,因此,探索涉及神经炎症的途径的作用非常重要。此外,非编码 RNA(ncRNAs)的重要性,如 microRNAs(miRNAs)、长非编码 RNA(lncRNAs)和竞争性内源 RNA(ceRNAs),已经被广泛研究,重点是 PD 的发病机制。然而,尽管近年来将 ncRNAs 与神经炎症途径和氧化应激联系起来的研究数量显著增加,但仍没有关于神经炎症相关 ncRNAs 作为 PD 发病机制中潜在生物标志物和治疗靶点的综合综述。因此,本综述旨在描述调节性 ncRNAs 与 PD 神经炎症靶点之间的相互作用,以发现和提出临床中新型联合生物标志物或治疗靶点。

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本文引用的文献

1
Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases.非编码RNA:神经退行性疾病中的神经炎症调节因子
Front Neurol. 2022 Aug 12;13:929290. doi: 10.3389/fneur.2022.929290. eCollection 2022.
2
A novel approach to type 3 diabetes mechanism: The interplay between noncoding RNAs and insulin signaling pathway in Alzheimer's disease.一种新型的 3 型糖尿病发病机制研究方法:非编码 RNA 与阿尔茨海默病胰岛素信号通路的相互作用。
J Cell Physiol. 2022 Jul;237(7):2838-2861. doi: 10.1002/jcp.30779. Epub 2022 May 17.
3
Biomarker of Neuroinflammation in Parkinson's Disease.
帕金森病神经炎症的生物标志物。
Int J Mol Sci. 2022 Apr 8;23(8):4148. doi: 10.3390/ijms23084148.
4
Paraquat-induced oxidative stress regulates N6-methyladenosine (mA) modification of long noncoding RNAs in Neuro-2a cells.百草枯诱导的氧化应激调节神经细胞 N6-甲基腺苷(mA)修饰的长链非编码 RNA。
Ecotoxicol Environ Saf. 2022 Jun 1;237:113503. doi: 10.1016/j.ecoenv.2022.113503. Epub 2022 Apr 19.
5
MicroRNAs Play a Role in Parkinson's Disease by Regulating Microglia Function: From Pathogenetic Involvement to Therapeutic Potential.微小RNA通过调节小胶质细胞功能在帕金森病中发挥作用:从发病机制到治疗潜力
Front Mol Neurosci. 2022 Jan 21;14:744942. doi: 10.3389/fnmol.2021.744942. eCollection 2021.
6
Long non-coding RNA myocardial infarction-associated transcript promotes 1-Methyl-4-phenylpyridinium ion-induced neuronal inflammation and oxidative stress in Parkinson's disease through regulating microRNA-221-3p/ transforming growth factor /nuclear factor E2-related factor 2 axis.长链非编码 RNA 心肌梗死相关转录物通过调节 microRNA-221-3p/转化生长因子/核因子 E2 相关因子 2 轴促进 1-甲基-4-苯基吡啶离子诱导的帕金森病神经元炎症和氧化应激。
Bioengineered. 2022 Jan;13(1):930-940. doi: 10.1080/21655979.2021.2015527.
7
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J Biomed Sci. 2021 Nov 18;28(1):78. doi: 10.1186/s12929-021-00775-x.
8
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Bioengineered. 2021 Dec;12(2):12867-12879. doi: 10.1080/21655979.2021.2005928.
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10
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J Cell Physiol. 2022 Feb;237(2):1206-1224. doi: 10.1002/jcp.30624. Epub 2021 Nov 1.