Evidence map›Paper›PMID 40518534›Full record

ArticleItalian journal of pediatrics2025

The dysregulation and regulatory mechanism of long non-coding RNA LBX2-AS1 in children with epilepsy.

Qian Li, Ning Li

Abstract read
In one paragraph

Article in Italian journal of pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. The Heterogeneous Nuclear Ribonucleoprotein K (Animals : an open access journal from MDPI · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Qian LiDepartment of Paediatric, Dongying People's Hospital, No. 317, Dongcheng South 1st Road, Dongying, 257091, China. liqiandr@163.com.ORCID http://orcid.org/0009-0001-5993-7186
Ning LiDepartment of Surgery, Guangrao County Traditional Chinese Medicine Hospital, Dongying, 257399, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpilepsy is a long-lasting neurological condition distinguished by recurring seizures, and related to oxidative stress and inflammation. This study investigates the effects of long non-coding RNA LBX2-AS1 on childhood epilepsy.

methodsThere were 165 epilepsy epileptic and 206 healthy children enrolled in this study. Relative LBX2-AS1, miR-873-5p, and HNRNPK expression levels were assessed using RT-PCR. Diagnostic value of LBX2-AS1 was evaluated by ROC curve. Epilepsy cell model was constructed in HT22 cells. Cell viability was assessed by CCK-8 kit. Cell apoptosis was analyzed by flow cytometer. Oxidative stress factors (SOD, GSH, LDH) and inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated by ELISA kits. Target association was validated using dual-luciferase reporter assays. Function analysis for miR-873-5p target genes was analyzed by GO, KEGG, and PPI.

resultsLBX2-AS1 was upregulated in epilepsy and had a high diagnostic value for epilepsy (AUC = 0.880, sensitivity = 80.6%, specificity = 82.0%, cutoff value = 1.14). The upregulation of LBX2-AS1 in cell model might decrease cell viability, increase apoptosis, and elevate oxidative stress and inflammation via negatively controlled miR-873-5p. Target genes of miR-873-5p were enriched in pathways related to oxidative stress, inflammation responses, and magnesium ion transmembrane transporter activity of neuronal cells. HNRNPK had the highest interaction degree with other target genes.

conclusionLBX2-AS1 is upregulated in epilepsy and is associated with increased oxidative stress, inflammation, and apoptosis via mediating miR-873-5p/HNRNPK axis in epilepsy cell model.

Indexed as

EpilepsyRNA, Long NoncodingAdolescentApoptosisCase-Control StudiesChildChild, PreschoolFemaleHumansMaleMicroRNAsOxidative StressUp-RegulationMicroRNAsRNA, Long NoncodingEpilepsyInflammationLBX2-AS1Oxidative stress

Identifiers

PMID40518534
PMCPMC12168281

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.