The mechanistic view of non-coding RNAs as a regulator of inflammatory pathogenesis of Parkinson's disease

被引:1
|
作者
Li, Yu'an [1 ]
Yu, Chunlei [1 ]
Jiang, Xiaobing [1 ]
Fu, Jia [1 ]
Sun, Ning [1 ]
Zhang, Daquan [1 ]
机构
[1] Jilin Prov FAW Gen Hosp, Dept Neurosurg, Changchun 130000, Peoples R China
关键词
Parkinson's disease; Inflammation; ncRNAs; miRNAs; circRNAs; lncRNAs; NLRP3; ALPHA-SYNUCLEIN OLIGOMERS; MITOCHONDRIAL COMPLEX-I; SUBSTANTIA-NIGRA; PHARMACOLOGICAL-TREATMENT; MICROGLIAL ACTIVATION; PROTEASOMAL FUNCTION; SIRNA DELIVERY; STEM-CELLS; MPTP MODEL; NEURODEGENERATION;
D O I
10.1016/j.prp.2024.155349
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to motor and non-motor symptoms. Emerging evidence suggests that inflammation plays a crucial role in the pathogenesis of PD, with the NLRP3 inflammasome implicated as a key mediator. Nfon-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have recently garnered attention for their regulatory roles in various biological processes, including inflammation. This review aims to provide a mechanistic insight into how ncRNAs function as regulators of inflammatory pathways in PD, with a specific focus on the NLRP3 inflammasome. We discuss the dysregulation of miRNAs and lncRNAs in PD pathogenesis and their impact on neuroinflammation through modulation of NLRP3 activation, cytokine production, and microglial activation. Additionally, we explore the crosstalk between ncRNAs, alpha-synuclein pathology, and mitochondrial dysfunction, further elucidating the intricate network underlying PD-associated inflammation. Understanding the mechanistic roles of ncRNAs in regulating inflammatory pathways may offer novel therapeutic targets for the treatment of PD and provide insights into the broader implications of ncRNA-mediated regulation in neuroinflammatory diseases.
引用
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页数:15
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