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沉默癫痫风暴:靶向星形胶质细胞和小胶质细胞中的miRNA-lncRNA相互作用以消除神经炎症触发因素。

Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers.

作者信息

Meng Jing, Luo Wen, Zhang Nana, Yu Mingxing, He Yuxuan, Chen Chunyan, Shu Haifeng, Yu Liang

机构信息

Department of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.

Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.

出版信息

Front Mol Neurosci. 2025 Jul 28;18:1616804. doi: 10.3389/fnmol.2025.1616804. eCollection 2025.

DOI:10.3389/fnmol.2025.1616804
PMID:40791576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12336184/
Abstract

Epilepsy is a chronic neurological disorder characterized by abnormal synchronous discharges of neurons in the brain. It affects approximately 70 million people worldwide, and approximately 30% of patients are resistant to existing antiepileptic drugs. Repeated seizures can lead to neuronal damage, glial cell activation and neuroinflammation, creating a vicious cycle of seizures, inflammation, and neuronal damage. Recent studies have shown that microRNAs play a key role in the pathological process of epilepsy by regulating the phenotype, inflammatory response and metabolic function of astrocytes and microglia. In addition, long noncoding RNAs, as upstream regulators of miRNAs, influence miRNA function by acting as competitive endogenous RNAs, further regulating glial cell activation and inflammatory responses. This paper is the first to systematically elucidate the synergistic role of miRNAs and lncRNAs in epilepsy through glial cell polarization, metabolic imbalance and exosome-mediated transcellular communication, providing a theoretical framework for the development of multitargeted intervention strategies.

摘要

癫痫是一种慢性神经系统疾病,其特征是大脑中神经元异常同步放电。全球约有7000万人受其影响,约30%的患者对现有的抗癫痫药物耐药。反复癫痫发作可导致神经元损伤、胶质细胞激活和神经炎症,形成癫痫发作、炎症和神经元损伤的恶性循环。最近的研究表明,微小RNA通过调节星形胶质细胞和小胶质细胞的表型、炎症反应和代谢功能,在癫痫的病理过程中起关键作用。此外,长链非编码RNA作为微小RNA的上游调节因子,通过充当竞争性内源性RNA影响微小RNA功能,进一步调节胶质细胞激活和炎症反应。本文首次通过胶质细胞极化、代谢失衡和外泌体介导的跨细胞通讯,系统阐明了微小RNA和长链非编码RNA在癫痫中的协同作用,为多靶点干预策略的开发提供了理论框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/994ca711efa9/fnmol-18-1616804-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/b8ad438fc82a/fnmol-18-1616804-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/d7511de7c105/fnmol-18-1616804-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/9d76ad5faad0/fnmol-18-1616804-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/994ca711efa9/fnmol-18-1616804-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/b8ad438fc82a/fnmol-18-1616804-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/d7511de7c105/fnmol-18-1616804-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/9d76ad5faad0/fnmol-18-1616804-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5337/12336184/994ca711efa9/fnmol-18-1616804-g004.jpg

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本文引用的文献

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J Exp Clin Cancer Res. 2025 Apr 21;44(1):126. doi: 10.1186/s13046-025-03391-x.
2
Purinergic receptor antagonism reduces interictal discharges and rescues cognitive function in a mouse model of temporal lobe epilepsy.嘌呤能受体拮抗作用可减少颞叶癫痫小鼠模型的发作间期放电并挽救认知功能。
Front Neurosci. 2025 Apr 4;19:1513135. doi: 10.3389/fnins.2025.1513135. eCollection 2025.
3
Targeted miRNA Delivery in Epilepsy: Mechanisms, Advances, and Therapeutic Potential.
癫痫中的靶向性微小RNA递送:机制、进展及治疗潜力
Mol Biol Rep. 2025 Apr 7;52(1):368. doi: 10.1007/s11033-025-10436-z.
4
Astroglia's role in synchronized spontaneous neuronal activity: from physiology to pathology.星形胶质细胞在同步性自发神经元活动中的作用:从生理学到病理学
Front Cell Neurosci. 2025 Mar 19;19:1544460. doi: 10.3389/fncel.2025.1544460. eCollection 2025.
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Neuroglia in epilepsy.癫痫中的神经胶质细胞
Handb Clin Neurol. 2025;210:69-86. doi: 10.1016/B978-0-443-19102-2.00016-8.
6
The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.神经炎症和网络异常在耐药性癫痫中的作用
Neurosci Bull. 2025 May;41(5):881-905. doi: 10.1007/s12264-025-01348-w. Epub 2025 Feb 24.
7
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