ArticleMolecular and cellular biochemistry2024
Investigating the expression level of miR-17-3p, miR-101-3p, miR-335-3p, and miR-296-3p in the peripheral blood of patients with acute myocardial infarction.
Article in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- LncRNA FTX promotes myocardial fibrosis by sponging miR-335-3p to regulate TFEC/ILK signaling.Scientific reports · 2026Article
- The Phoenix Heart-PICSO and the Rebirth of Embryonic Life in the Ischemic Myocardium.Journal of cardiovascular development and disease · 2026Review
- Dysregulation of miRNAs in Sicilian Patients with Autism Spectrum Disorder.Biomedicines · 2026Article
- Upregulation of miR-17-3p is associated with HbF in patients with β-thalassemia and induces γ-globin expression by targeting BCL11A.Orphanet journal of rare diseases · 2025Article
- A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
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Abstract
The role of inflammation has been proven in acute myocardial infarction (AMI) pathogenesis. Due to the effect of NLRP3 gene expression in the inflammation process of MI, we aimed to explore the expression changes and diagnostic power of four inflammation-related miRNAs including miR-17-3p, miR-101-3p, miR-335-3p, miR-296-3p and their potential target, NLRP3, in ST-segment elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI) patients as two major classes of AMI. The expression level of these genes were evaluated in 300 participants equally divided into three groups of STEMI, NSTEMI, and control using quantitative real-time PCR. The expression level of NLRP3 was upregulated in STEMI and NSTEMI patients compared to control subjects. Besides, the expression levels of miR-17-3p, miR-101-3p, and miR-296-3p were significantly downregulated in STEMI and NSTEMI patients compared to controls. The increased expression of NLRP3 had a very strong inverse correlation with miR-17-3p in patients with STEMI and with miR-101-3p in the STEMI and NSTEMI patients. ROC curve analysis showed that the expression level of miR-17-3p had the highest diagnostic power for discrimination between STEMI patients and controls. Remarkably, the combination of all markers resulted in a higher AUC. In summary, there is a significant association between the expression levels of miR-17-3p, miR-101-3p, miR-335-3p, miR-296-3p, and NLRP3 and the incidence of AMI. Although the miR-17-3p expression level has the highest diagnostic power to distinguish between STEMI patients and control subjects, the combination of these miRNAs and NLRP3 could serve as a novel potential diagnostic biomarker of STEMI.
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