ArticleMetabolic brain disease2026
LINC01094 exacerbates acute cerebral infarction by regulating miR-499a-5p.
Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study is to clarify the role of LINC01094 in acute cerebral infarction (ACI) and to explore its potential molecular mechanisms. A total of 121 patients with ACI and 133 healthy controls were enrolled in this study. The expression levels of LINC01094, miR-499a-5p, and inflammatory markers (CRP, IL-6) were measured using RT-qPCR. The levels of MDA, SOD, and ROS were measured using commercial assay kits. The diagnostic value of LINC01094 for ACI was evaluated using ROC curve analysis. CCK-8 assay and flow cytometry were utilized to measure cell viability and apoptosis. The subcellular localization of LINC01094 in SH-SY5Y cells was determined. The predicted targeting relationship between LINC01094 and miR-499a-5p was validated using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Serum LINC01094 expression was significantly elevated in ACI patients and demonstrated diagnostic value for ACI. miR-499a-5p expression was markedly reduced in both ACI patients and in vitro/in vivo models, showing a significant negative correlation with LINC01094 expression in patients. Downregulation LINC01094 mitigated OGD/R-induced damage in SH-SY5Y cells and cerebral injury in MCAO rats, while inhibition miR-499a-5p reversed this protective effect. Furthermore, CACNB2 was confirmed as a direct target of miR-499a-5p. LINC01094 participates in the pathological process of ACI injury by competitively binding to and inhibiting the activity of miR-499a-5p. These findings suggest that LINC01094 may serve as a potential therapeutic target for ACI treatment.
Indexed as
Identifiers
42250179What Socratic holds
Registered trials
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 Socratic graph.