ArticleJournal of cardiothoracic surgery2025
Study on the mechanism and clinical value of miR-210-3p and miR-582-5p in acute myocardial infarction by targeting MXD1.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Predictive Biomarkers for Coronary Collateral Circulation Development After Myocardial Infarction.International journal of molecular sciences · 2026Review
- MicroRNA Signatures in Cardiometabolic Disorders as a Next-Generation Diagnostic Approach: Current Insight.International journal of molecular sciences · 2025Review
- Effects of miR-210-3p/SDF2 and miR-31-5p/FGF7 from hypoxic endometrial exosomes on UCB-MSC proliferation, migration, and differentiation.Stem cell research & therapy · 2025Article
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3 authors.
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Abstract
backgroundAcute myocardial infarction (AMI) occurs rapidly and is a major cause of death in patients with coronary artery disease (CAD). To explore new biomarkers of AMI and its pathogenesis.
methodsMining key miRNAs (miR-210-3p, miR-582-5p) and gene (MXD1) using the GEO and starbase databases. The expression of miRNAs and related genes was detected by qPCR. The clinical value of miR-210-3p/miR-582-5p was evaluated by constructing ROC curves. The targeted regulation of MXD1 by miR-210-3p and miR-582-5p was demonstrated by the dual-luciferase assay and transfection of mimics. The levels of cTnI, MDA, and Fe
resultsMiR-210-3p and miR-582-5p were deficient in AMI patients and hypoxic cardiomyocytes, while MXD1 was high-expressed. MiR-210-3p combined with miR-582-5p could well distinguish ST elevation-AMI and non-ST elevation-AMI patients from CAD patients, with AUC of 0.865 (0.806-0.923) and 0.813 (0.744-0.881), respectively. The mimics of miR-210-3p and miR-582-5p significantly reduced luciferase activity in cells transfected with the wild-type luciferase vector of MXD1 and inhibited MXD1 expression, which was promoted by their inhibitors. Overexpression of miR-210-3p/miR-582-5p saved hypoxia-induced ferroptosis, which was reversed by co-transfection of the MXD1 plasmid.
conclusionMiR-210-3p and miR-582-5p are good classifiers for AMI patients and CAD patients. They can negatively regulate the expression of MXD1 by directly targeting its mRNA, inhibiting ferroptosis of hypoxic cardiomyocytes, and may be effective predictors of CAD progression to AMI.
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