Abstract | OBJECTIVE: METHODS: Plasma miR-223 and miR-126 levels were measured before treatment. Treatment responses and 2-year survival were determined. In vitro experiments were performed to explore the mechanism of action. RESULTS: Patients with resistance to DAPT had a lower level of miR-223 and miR-126. Cardiac-event-free survival was shorter in patients with lower miR-223 or miR-126 levels. MiR-223 and miR-126 independently predicted DAPT resistance. Modulating miR-223 or miR-126 in platelets in vitro significantly changed the response to clopidogrel by regulating platelet aggregation. CONCLUSION: MiR-223 and miR-126 play a role in DAPT resistance and may provide potential biomarkers in patients with STEMI.
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Authors | Xiaojing Li, Qi Yao, Hanbin Cui, Jun Yang, Nan Wu, Yahui Liu, Ying Zhou, Yinwei Zhang, Jia Su, Yezi Xia, Xiaomin Chen |
Journal | The Journal of international medical research
(J Int Med Res)
Vol. 49
Issue 6
Pg. 3000605211016209
(Jun 2021)
ISSN: 1473-2300 [Electronic] England |
PMID | 34098766
(Publication Type: Journal Article)
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Chemical References |
- MIRN126 microRNA, human
- MIRN223 microRNA, human
- MicroRNAs
- Platelet Aggregation Inhibitors
- Clopidogrel
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Topics |
- Blood Platelets
- Clopidogrel
(therapeutic use)
- Humans
- MicroRNAs
(genetics)
- Percutaneous Coronary Intervention
- Platelet Aggregation Inhibitors
(therapeutic use)
- ST Elevation Myocardial Infarction
(drug therapy, genetics)
- Treatment Outcome
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