Construction and analysis of a competing endogenous RNA network associated with circRNAs dysregulated in medial temporal lobe epilepsy

Li, Kelu; Wu, Chongmin; Zhu, Yongyun; Yin, Weifang; Ren, Hui; Yang, Xinglong

doi:10.1684/epd.2021.1403

Cited by 4 publications

(1 citation statement)

References 44 publications

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“…Via bioinformatics technology, researchers used Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) network to reveal that synapses play a crucial role in medial temporal lobe epilepsy (MTLE) [ 23 ]. It has been reported that the changes of postsynaptic glutamate receptor increase the excitability of hippocampal neural network, and 4-aminopyridine (4-AP) -induced epileptiform activity in hippocampal brain slices of rat in vitro model shows that alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/N-methyl-D-aspartate (NMDA) ratio increases [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

Shan

Chen

et al. 2023

Neurochem Res

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Epilepsy is a common and severe neurological disorder in which impaired glucose metabolism leads to changes in neuronal excitability that slow or promote the development of epilepsy. Leptin and adiponectin are important mediators regulating glucose metabolism in the peripheral and central nervous systems. Many studies have reported a strong association between epilepsy and these two adipokines involved in multiple signaling cascades and glucose metabolism. Due to the complex regulatory mechanisms between them and various signal activation networks, their role in epilepsy involves many aspects, including the release of inflammatory mediators, oxidative damage, and neuronal apoptosis. This paper aims to summarize the signaling pathways involved in leptin and adiponectin and the regulation of glucose metabolism from the perspective of the pathogenesis of epilepsy. In particular, we discuss the dual effects of leptin in epilepsy and the relationship between antiepileptic drugs and changes in the levels of these two adipokines. Clinical practitioners may need to consider these factors in evaluating clinical drugs. Through this review, we can better understand the specific involvement of leptin and adiponectin in the pathogenesis of epilepsy, provide ideas for further exploration, and bring about practical significance for the treatment of epilepsy, especially for the development of personalized treatment according to individual metabolic characteristics.

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Section: Introductionmentioning

confidence: 99%

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

Shan

Chen

et al. 2023

Neurochem Res

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The identification of biomarkers for Alzheimer's disease using a systems biology approach based on lncRNA-circRNA-miRNA-mRNA ceRNA networks

Sokouti

2024

Computers in Biology and Medicine

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Emerging roles of long non‐coding RNAs in human epilepsy

Yazarlou,

Lipovich,

Loeb

2024

Epilepsia

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Genome‐scale biological studies conducted in the post‐genomic era have revealed that two‐thirds of human genes do not encode proteins. Most functional non‐coding RNA transcripts in humans are products of long non‐coding RNA (lncRNA) genes, an abundant but still poorly understood class of human genes. As a result of their fundamental and multitasking regulatory roles, lncRNAs are associated with a wide range of human diseases, including neurological disorders. Approximately 40% of lncRNAs are specifically expressed in the brain, and many of them exhibit distinct spatiotemporal patterns of expression. Comparative genomics approaches have determined that 65%–75% of human lncRNA genes are primate‐specific and hence can be posited as a contributing potential cause of the higher‐order complexity of primates, including human, brains relative to those of other mammals. Although lncRNAs present important mechanistic examples of epileptogenic functions, the human/primate specificity of lncRNAs questions their relevance in rodent models. Here, we present an in‐depth review that supports the contention that human lncRNAs are direct contributors to the etiology and pathogenesis of human epilepsy, as a means to accelerate the integration of lncRNAs into clinical practice as potential diagnostic biomarkers and therapeutic targets. Meta‐analytically, the major finding of our review is the commonality of lncRNAs in epilepsy and cancer pathogenesis through mitogen‐activated protein kinase (MAPK)‐related pathways. In addition, neuroinflammation may be a relevant part of the common pathophysiology of cancer and epilepsy. LncRNAs affect neuroinflammation‐related signaling pathways such as nuclear factor kappa‐ light‐ chain‐ enhancer of activated B cells (NF‐κB), Notch, and phosphatidylinositol 3‐ kinase/ protein kinase B (Akt) (PI3K/AKT), with the NF‐κB pathway being the most common. Besides the controversy over lncRNA research in non‐primate models, whether neuroinflammation is triggered by injury and/or central nervous system (CNS) toxicity during epilepsy modeling in animals or is a direct consequence of epilepsy pathophysiology needs to be considered meticulously in future studies.

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Construction and analysis of a competing endogenous RNA network associated with circRNAs dysregulated in medial temporal lobe epilepsy

Cited by 4 publications

References 44 publications

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

The identification of biomarkers for Alzheimer's disease using a systems biology approach based on lncRNA-circRNA-miRNA-mRNA ceRNA networks

Emerging roles of long non‐coding RNAs in human epilepsy

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