ArticleBiochemical genetics2025
miR-432-5p Targeting SORT1 to Protect Artery Smooth Muscle Cells and Inhibit Coronary Artery Disease.
Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- The Mechanism and Diagnostic Value of the LINC01220/hsa-miR- 6727 - 5p/FBLN5 Axis in Coronary Atherosclerosis.Biochemical genetics · 2026Article
- Twenty-five years of WWOX insight in cancer: a treasure trove of knowledge.Functional & integrative genomics · 2025Review
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
Recent studies highlight the crucial role of microRNAs (miRNAs) in coronary artery disease (CAD). This retrospective study investigated the abundance of miR-432-5p in the serum of CAD patients and explored its role. 252 volunteers were included. The levels of miR-432-5p and Sortilin 1 (SORT1) in the serum of CAD patients and oxidized low-density lipoprotein (ox-LDL)-treated human arterial smooth muscle cells (HASMCs) were quantified via qRT-PCR. The correlation coefficient, clinical diagnostic performance, and risk factors were analyzed with Pearson correlation, receiver operating characteristic (ROC) curve, and binomial logistic regression, respectively. HASMC proliferation, migration, and apoptosis were evaluated using Cell Counting Kit-8 (CCK-8), transwell, and flow cytometry assay, respectively. Potential binding sites between miR-432-5p and SORT1 were predicted with TargetScan and validated through dual-luciferase reporter assay and co-transfection experiments. Serum miR-432-5p was decreased, while SORT1 was elevated in CAD patients and ox-LDL-induced HASMCs. miR-432-5p showed a negative correlation with total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), C-reactive protein (CRP), and Gensini score. miR-432-5p and SORT1 effectively distinguished CAD patients from controls based on ROC analysis. miR-432-5p and SORT1 serve as independent risk predictors. Restoration of miR-432-5p reversed ox-LDL-induced increases in HASMC proliferation and migration and restored apoptosis levels. SORT1 was confirmed as a direct target of miR-432-5p, and its upregulation counteracted the protective effects of miR-432-5p on HASMC under ox-LDL exposure. This study suggests that miR-432-5p protects HASMCs and inhibits coronary artery disease progression by targeting SORT1, positioning both miR-432-5p and SORT1 as potential biomarkers for CAD.
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Identifiers
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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.