Evidence map›Paper›PMID 42131328›Full record

ArticleFrontiers in immunology2026

miR-511-3p dysregulation-mediated AKT3/USP8 signaling imbalance: a molecular bridge between neuroinflammation and PSCI.

Wei Zhao, Kangping Song, Fen Yang, Hui Xiao, Yan Liu, Yachun Yu, Te Wang

Abstract read
In one paragraph

Article in Frontiers in immunology, 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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0citing papers in PubMed
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1 · What the graph read from it

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.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Wei Zhao *Department of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Kangping Song *Department of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Fen YangDepartment of Science and Education, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Hui XiaoDepartment of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Yan LiuDepartment of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Yachun YuDepartment of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Te WangDepartment of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study aims to explore the regulatory effect of miR-511-3p expression imbalance on the AKT3/USP8 signaling pathway, as well as the "molecular bridge" function of this signaling imbalance between neuroinflammation and post-stroke cognitive impairment (PSCI). Methods: 118 stroke patients and 80 healthy individuals were enrolled. Bioinformatics and dual-luciferase assays confirmed miR-511-3p - AKT3 interaction. Oxygen-glucose deprivation/reoxygenation (OGD/R) established a stroke inflammatory cell model. Inflammatory cytokines were measured via ELISA. RT-qPCR detected miR-511-3p, AKT3, and USP8 expressions. Correlation analysis and risk factor analysis were performed using Pearson correlation and logistic regression. Results: This study found that AKT3 was a direct target of miR-511-3p. In the neural inflammation cell model, miR-511-3p could regulate the expression of AKT3/USP8; miR-511-3p/AKT3/USP8 could regulate the inflammatory response in the inflammatory cell model. In the serum of PSCI patients, the expression of miR-511-3p and USP8 were decreased, while the expressions of AKT3 was increased, and all three were associated with the inflammatory factors of the patients. Logistic regression analysis showed that low expression of miR-511-3p and USP8 were independent risk factors for PSCI. Conclusion: miR-511-3p may regulate the expression of USP8 by targeting AKT3, thereby influencing the neuroinflammatory response and participating in the occurrence and development of PSCI. miR-511-3p and USP8 may potentially serve as biomarkers and therapeutic targets for PSCI.

Indexed as

EndopeptidasesEndosomal Sorting Complexes Required for TransportMicroRNAsNeuroinflammatory DiseasesProto-Oncogene Proteins c-aktStrokeUbiquitin ThiolesteraseAgedFemaleGene Expression RegulationHumansMaleMiddle AgedSignal TransductionAKT3 protein, humanEndopeptidasesEndosomal Sorting Complexes Required for TransportMicroRNAsMIRN511 microRNA, humanProto-Oncogene Proteins c-aktUbiquitin ThiolesteraseUSP8 protein, humanAKT3inflammatory responsesmiR-511-3pneuroinflammationpost-stroke cognitive impairmentstrokeUSP8

Identifiers

PMID42131328
PMCPMC13160869

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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.