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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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http://dx.doi.org/10.1515/revneuro-2025-0041 | DOI Listing |
Alzheimers Res Ther
September 2025
Department of Neurology, Saarland University, Kirrberger Straße, 66421, Homburg/Saar, Germany.
Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.
View Article and Find Full Text PDFBioimpacts
August 2025
Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan 420008, Russia.
Introduction: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS). CD4 CD25 Tregs, which normally suppress immune responses, exhibit impaired function in MS. Treg-derived extracellular vesicles (EVs) carry immunoregulatory proteins and miRNAs that modulate T-cell activity.
View Article and Find Full Text PDFExp Clin Endocrinol Diabetes
August 2025
Department of Endocrinology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, China.
Painful diabetic neuropathy (PDN), a severe microvascular complication of diabetes, is closely associated with neuroinflammation. This study aimed to investigate the mechanism of circ_0002590 in neuroinflammation associated with PDN.The Schwann cells (HEI193) were treated with high glucose (HG, 150 mM) to simulate the diabetic microenvironment.
View Article and Find Full Text PDFPLoS One
September 2025
Orthopaedics, Hebei Medical University Third Hospital, Shijiazhuang, China.
Enoxaparin sodium (ES), a low molecular weight heparin derivative, has recently been recognized for its diverse biological activities. In particular, the ability of heparin to modulate inflammation has been utilized to enhance the biocompatibility of bone implant materials. In this study, we utilized poly (methyl methacrylate) (PMMA), a drug loading bone implant material, as a matrix and combined this with enoxaparin sodium (ES) to create enoxaparin sodium PMMA cement (ES-PMMA) to investigate the regulatory effects of ES on inflammatory responses in bone tissue from an animal model.
View Article and Find Full Text PDFCell Mol Life Sci
September 2025
Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
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