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Blood. 2022 May 26;139(21):3181-3193. doi: 10.1182/blood.2021012048.
2
The Role of Brain-Derived Neurotrophic Factor in Epileptogenesis: an Update.脑源性神经营养因子在癫痫发生中的作用:最新进展
Front Pharmacol. 2021 Nov 26;12:758232. doi: 10.3389/fphar.2021.758232. eCollection 2021.
3
Expression of 4E-BP1 in juvenile mice alleviates mTOR-induced neuronal dysfunction and epilepsy.4E-BP1 在幼年小鼠中的表达可减轻 mTOR 诱导的神经元功能障碍和癫痫。
Brain. 2022 May 24;145(4):1310-1325. doi: 10.1093/brain/awab390.
4
MicroRNA-124: A Key Player in Microglia-Mediated Inflammation in Neurological Diseases.微小RNA-124:神经疾病中小胶质细胞介导的炎症反应中的关键因子
Front Cell Neurosci. 2021 Nov 2;15:771898. doi: 10.3389/fncel.2021.771898. eCollection 2021.
5
Clinical value of lncRNA TUG1 in temporal lobe epilepsy and its role in the proliferation of hippocampus neuron via sponging miR-199a-3p.长链非编码 RNA TUG1 在颞叶癫痫中的临床价值及其通过海绵吸附 miR-199a-3p 促进海马神经元增殖的作用。
Bioengineered. 2021 Dec;12(2):10666-10673. doi: 10.1080/21655979.2021.2001904.
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Capsaicin Protects Against Lipopolysaccharide-Induced Acute Lung Injury Through the HMGB1/NF-κB and PI3K/AKT/mTOR Pathways.辣椒素通过HMGB1/NF-κB和PI3K/AKT/mTOR信号通路对脂多糖诱导的急性肺损伤具有保护作用。
J Inflamm Res. 2021 Oct 14;14:5291-5304. doi: 10.2147/JIR.S309457. eCollection 2021.
7
Preimplantation factor modulates oligodendrocytes by H19-induced demethylation of NCOR2.植入前因子通过 H19 诱导的 NCOR2 去甲基化调节少突胶质细胞。
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8
LncRNA MALAT1 promotes breast cancer progression by sponging miR101-3p to mediate mTOR/PKM2 signal transmission.长链非编码RNA MALAT1通过吸附miR101-3p介导mTOR/PKM2信号传导来促进乳腺癌进展。
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mTOR 信号与非编码 RNA 在调控癫痫性神经炎症中的协同作用。

The Coordination of mTOR Signaling and Non-Coding RNA in Regulating Epileptic Neuroinflammation.

机构信息

Departments of Neurosurgery, and National Clinical Research Center of Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.

Department of Neonatology, Yale School of Medicine, New Haven, CT, United States.

出版信息

Front Immunol. 2022 Jul 11;13:924642. doi: 10.3389/fimmu.2022.924642. eCollection 2022.

DOI:10.3389/fimmu.2022.924642
PMID:35898503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9310657/
Abstract

Epilepsy accounts for a significant proportion of the burden of neurological disorders. Neuroinflammation acting as the inflammatory response to epileptic seizures is characterized by aberrant regulation of inflammatory cells and molecules, and has been regarded as a key process in epilepsy where mTOR signaling serves as a pivotal modulator. Meanwhile, accumulating evidence has revealed that non-coding RNAs (ncRNAs) interfering with mTOR signaling are involved in neuroinflammation and therefore articipate in the development and progression of epilepsy. In this review, we highlight recent advances in the regulation of mTOR on neuroinflammatory cells and mediators, and feature the progresses of the interaction between ncRNAs and mTOR in epileptic neuroinflammation.

摘要

癫痫占神经障碍负担的很大一部分。神经炎症是对癫痫发作的炎症反应,其特征是炎症细胞和分子的异常调节,已被认为是癫痫的关键过程,其中 mTOR 信号作为关键调节剂。同时,越来越多的证据表明,干扰 mTOR 信号的非编码 RNA(ncRNA)参与神经炎症,因此参与癫痫神经炎症的发生和发展。在这篇综述中,我们强调了 mTOR 对神经炎症细胞和介质的调节的最新进展,并介绍了 ncRNA 和 mTOR 在癫痫神经炎症中的相互作用的进展。