Inflammation-related microRNA alterations in epilepsy: a systematic review of human and animal studies
Rattachement africain : ir, in, gb, us. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Epilepsy is a neurological condition that affects around 50 million people globally. While the underlying mechanism of epilepsy is not fully understood, emerging evidence demonstrates that inflammation is a key player in the pathogenesis of epilepsy. MicroRNAs are involved in the pathogenesis of epilepsy, particularly through regulating oxidative stress, apoptosis, and inflammation. In this systematic review, we analyzed and summarized data from the literature regarding the role of inflammatory miRNAs in the pathophysiology of epilepsy, through human and animal studies. Twenty one reports on humans and 44 reports on animals were included in the current analysis. Kainic acid (KA) and pilocarpine were broadly used approaches in inducing epilepsy in animal models. Among upregulated microRNAs, miR-146a, miR-155, and miR-132 were more emphasized for their inflammatory role involved in epilepsy. MiR-221, miR-222, and miR-29a were downregulated and were associated with anti-inflammatory effects. Notably, microRNAs demonstrated tissue-specific expression patterns in different samples, including brain cortex, hippocampus, and body fluids, which is considerable in further investigations in the pathophysiologic and diagnostic roles of inflammatory microRNAs in epilepsy. Furthermore, inflammatory miRNAs regulate critical signaling pathways like TLR4/NF-κB, PI3K/Akt, and IL-1β-mediated neuroinflammation. Conclusively, these findings highlight the possibility of using inflammatory miRNAs as diagnostic biomarkers and therapeutic targets of epilepsies.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Inflammation-related microRNA alterations in epilepsy: a systematic review of human and animal studies
- Date Crossref
- 05/08/2025
- Éditeur
- Walter de Gruyter GmbH
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Les institutions déclarées
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