Evidence map›Paper›PMID 41327481›Full record

ArticleEuropean journal of medical research2025

MicroRNA-29b-3p promotes endothelial cell inflammation via NTRK2/PI3K/NLRP3 pathway in Moyamoya disease.

Liangzhe Wei, He Ren, Yuanwei Lin, Xinpeng Deng, Yuchun Liu, Jingjing Zeng, Jinghui Lin, Xiang Gao, Jie Sun, Yi Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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.

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

10 authors.

Liangzhe WeiNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China.
He RenNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China.
Yuanwei LinDepartment of Radiology, The First Affiliated Hospital of Ningbo University, Ningbo, 315000, Zhejiang, China.
Xinpeng DengDepartment of Neurosurgery, Beijing Hospital, National Center of Gerontology,, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Yuchun LiuNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China.
Jingjing ZengDepartment of Clinical Epidemiology, Ningbo No. 2 Hospital, Ningbo, 315000, China.
Jinghui LinNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China.
Xiang GaoNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China.
Jie SunNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China. fyysunjie@nbu.edu.cn.
Yi HuangNingbo Key Laboratory of Nervous System and Brain Function, Department of Neurosurgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, Zhejiang, China. huangy102@gmail.com.

Funding

Ningbo Clinical Research Center for Emergency and Critical Diseases 2024L003Ningbo Top Medical and Health Research Program 2022020304The Key Research and Development Program of Zhejiang Province 2024C03281(SD2)
6 · The paper itself

Abstract

Moyamoya disease (MMD) is a rare chronic progressive vascular anomaly of the skull base whose molecular regulatory mechanisms remain poorly understood. We therefore aimed to analyze the molecular mechanisms involved in the development of MMD from the perspective of miRNA regulation of mRNA. Raw gene expression profiles (GSE178501, GSE157628 and GSE189993) were downloaded from the Gene Expression Omnibus database and used to identify differentially expressed genes and perform functional enrichment analysis. Differentially expressed miRNAs and their predicted target genes were validated by RT-qPCR. Oxygen glucose deprivation was applied to induce an inflammatory injury cell model in human brain microvascular endothelial cells (BMEC). 973 differentially expressed mRNAs and 3 differentially expressed miRNAs were identified in three sets of gene expression profiles. RT-qPCR confirmed that the miR-29b-3p was upregulated in leukocytes of MMD and that the expression of NTRK2 was downregulated. Dual-luciferase reporter assay indicated that NTRK2 was the direct target of miR-29b-3p. Overexpression of NTRK2 improved the viability of BMEC and increased the protein levels of NTRK2 and pPI3K, while suppressed the expression of NLRP3, IL1β, and TNF-α. miR-29b-3p treatment partially abolished the protective effect of NTRK2 and diminished the effect of NTRK2 on PI3K/NLRP3 pathway. In conclusion, this study provided a novel insight into the pathophysiological mechanisms of MMD and demonstrated that the miR-29b-3p/NTRK2/PI3K/NLRP3 axis plays a pivotal role in the progression of MMD.

Indexed as

Endothelial CellsInflammationMicroRNAsMoyamoya DiseaseNLR Family, Pyrin Domain-Containing 3 ProteinPhosphatidylinositol 3-KinasesReceptor, trkBHumansMembrane GlycoproteinsSignal TransductionMembrane GlycoproteinsMicroRNAsMIRN29a microRNA, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPhosphatidylinositol 3-KinasesReceptor, trkBtropomyosin-related kinase-B, humanInflammationmiR-29b-3pMoyamoyaNLRP3NTRK2

Identifiers

PMID41327481
PMCPMC12772102

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.