Evidence map›Paper›PMID 42304299›Full record

ArticleBMC pediatrics2026

Clinical significance of LINC01093 in children with severe pneumonia and its regulation of miR‑326/MAPK1 axis.

Peng Tong, Na Wang

Abstract read
In one paragraph

Article in BMC pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Peng TongDepartment of Pediatrics, Ezhou Central Hospital, Ezhou, 436000, China.
Na WangDepartment of Pediatrics, Hengyang Central Hospital, No. 31, Guanghui Street, Huaxin Development Zone, Zhenxiang District, Hengyang City, Hubei Province, 421001, China. wangna_hy@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSevere pneumonia (SP) poses a significant threat to the life safety of children. This study aims to investigate the diagnostic and prognostic significance as well as the molecular mechanism of LINC01093 in children with SP.

methodsNinety-eight children with SP and ninety-two healthy children were included in the study. The diagnostic potential of LINC01093 was evaluated using the receiver operating characteristic (ROC) curve. The prognosis and the factors influencing the prognosis were analyzed through the Kaplan-Meier survival curve and the multivariate Cox regression model. An in vitro SP model was constructed by inducing MRC-5 cells with lipopolysaccharide (LPS). The relative expression of genes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and levels of inflammatory factors were detected by cell counting kit-8 (CCK-8), flow cytometry and Enzyme-linked immunosorbent assay (ELISA).

resultsCompared with healthy children, LINC01093 and MAPK1 were elevated in the serum of children with SP, while miR-326 was reduced. LINC01093 had a good diagnostic potential between children with SP and healthy children. High LINC01093 expression correlated with poor prognosis. Silencing LINC01093 upregulated the viability of MRC-5 cells induced by LPS, inhibited apoptosis and the levels of inflammatory factors (interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α)). Inhibiting miR-326 or overexpressing MAPK1 partially reversed the protective effect of LINC01093 silencing on LPS-induced cell damage.

conclusionSilencing LINC01093 exerts a protective effect against LPS-induced damage by regulating the miR-326/MAPK1 axis. This study provides new experimental evidence for understanding the pathogenesis of SP.

Indexed as

MicroRNAsMitogen-Activated Protein Kinase 1PneumoniaRNA, Long NoncodingApoptosisCase-Control StudiesCell LineCell SurvivalChildChild, PreschoolFemaleHumansInfantMalePrognosisSeverity of Illness IndexMAPK1 protein, humanMicroRNAsMIRN326 microRNA, humanMitogen-Activated Protein Kinase 1RNA, Long NoncodingLINC01093MAPK1miR-326Severe pneumonia

Identifiers

PMID42304299
PMCPMC13508191

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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.