Evidence map›Paper›PMID 40247354›Full record

ArticleJournal of cardiothoracic surgery2025

LncRNA MAGI2-AS3 promotes the progression of atherosclerosis by sponging miR-525-5p.

Lingfeng Zhu, Chan Yan

Abstract read
In one paragraph

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

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Lingfeng Zhu *Department of Cardiology, Shanghai Baoshan Aged-Nursing Hospital, No. 5425, Gonghexin Road, Baoshan District, Shanghai, 200443, China. zhulingfengsh@163.com.
Chan Yan *Department of Cardiology, Shanghai Baoshan Aged-Nursing Hospital, No. 5425, Gonghexin Road, Baoshan District, Shanghai, 200443, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence showed that lncRNAs are involved in the procession of atherosclerosis (AS). This study detected MAGI2-AS3 expression in the serum of AS patients and further investigated the mechanism of MAGI2-AS3 in AS.

methodsMAGI2-AS3 and miR-525-5p in the AS patients' serum and oxidized low-density lipoprotein (ox-LDL) induced human coronary artery smooth muscle cells (HCASMCs) were quantified by qRT-PCR. Spearman correlation was calculated between MAGI2-AS3 and clinical indexes or miR-525-5p. ROC curve analyzed the clinical diagnostic performance of MAGI2-AS3. Small interfering RNA targeting MAGI2-AS3 (si-MAGI2-AS3) silenced MAGI2-AS3 expression. HCASMCs proliferation, migration, and apoptosis were assayed by CCK-8, transwell, and flow cytometry, respectively. The target miR-525-5p was predicted by StarBase and verified by dual-luciferase reporter assay and co-transfection.

resultsMAGI2-AS3 increased in the AS patients' serum and ox-LDL-induced HCASMCs. MAGI2-AS3 was negatively associated with C-reactive protein (CRP) and carotid intima-media thickness (CIMT). The ROC curve confirmed the efficacy of MAGI2-AS3 in distinguishing AS from control subjects. Silencing MAGI2-AS3 reversed the enhancement of proliferation and migration and the reduction of apoptosis caused by ox-LDL in HCASMCs. MiR-525-5p was predicted as a target and further verified by dual-luciferase assay. MiR-525-5p declined in both the serum of AS patients and ox-LDL-induced HCASMCs. Rescue experiments showed that miR-525-5p downregulation inverted the decrease in proliferation and migration, and the increase in apoptosis due to si-MAGI2-AS3 treatment.

conclusionsIn summary, our study demonstrated that MAGI2-AS3 participates in AS progression by sponging the miR-525-5p, indicating that MAGI2-AS3 may be a potential biomarker of AS.

Indexed as

AtherosclerosisGene Expression RegulationMicroRNAsRNA, Long NoncodingAdaptor Proteins, Signal TransducingApoptosisCell MovementCell ProliferationCells, CulturedDisease ProgressionFemaleGuanylate KinasesHumansMaleMiddle AgedMuscle, Smooth, VascularAdaptor Proteins, Signal TransducingGuanylate KinasesMAGI2 protein, humanMicroRNAsRNA, Long NoncodingAtherosclerosisMAGI2-AS3miR-525-5pProgression

Identifiers

PMID40247354
PMCPMC12004554

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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.