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Long noncoding RNA MIAT regulates VSMC migration by sponging miR-326.
Article in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- MIAT: An important long non-coding RNA regulating cardiovascular and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2026Review
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ObjectiveThe current study aimed to investigate the role of the myocardial infarction-associated transcript (MIAT)/microRNA-326 (miR-326) axis in regulating the migration of vascular smooth muscle cells (VSMCs) during the progression of atherosclerosis (AS).MethodsBioinformatic analysis of MIAT and miR-326 in two AS-related GEO datasets was performed via the online web tool GEO2R. MIAT and miR-326 expression in 46 paired plasma samples and in oxidized low-density lipoprotein (ox-LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine the expression of monocyte chemotactic protein 1 (MCP-1) after diverse ox-LDL treatments. The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis. Transwell assays were performed to determine the changes in migration after different MIAT or miR-326 interventions. RNA-fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular localization of MIAT and miR-326. The targeted binding effect between MIAT and miR-326 was confirmed via a luciferase assay.ResultsMIAT was upregulated and miR-326 was downregulated in 46 plasma samples from patients with AS compared with those from patients without AS (non-AS). A negative correlation was found between MIAT and miR-326 (r = - 0.6591,
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Registered trials
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