期刊
JOURNAL OF CLINICAL MEDICINE
卷 10, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/jcm10112371
关键词
microRNA; cardiovascular disease; diabetes; mortality; antiplatelet therapy; platelet reactivity; Let-7e; miR-126; miR-223; miR-125a-3p
资金
- Polish Ministry of Science and Higher Education [0072/DIA/2017/46]
- Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Centre for Preclinical Research and Technology CEPT, Warsaw, Poland
The study found that the expression of miR-126 is a strong and independent predictor of long-term all-cause mortality among patients with T2DM. Additionally, miR-223, miR-126, and Let-7e show significant interactions with antiplatelet treatment regimens and clinical outcomes.
MicroRNAs are endogenous non-coding RNAs that are involved in numerous biological processes through regulation of gene expression. The aim of our study was to determine the ability of several miRNAs to predict mortality and response to antiplatelet treatment among T2DM patients. Two hundred fifty-two patients with diabetes were enrolled in the study. Among the patients included, 26 (10.3%) patients died within a median observation time of 5.9 years. The patients were receiving either acetylsalicylic acid (ASA) 75 mg (65%), ASA 150 mg (15%) or clopidogrel (19%). Plasma miR-126, miR-223, miR-125a-3p and Let-7e expressions were assessed by quantitative real time PCR and compared between the patients who survived and those who died. Adjusted Cox-regression analysis was used for prediction of mortality. Differential miRNA expression due to different antiplatelet treatment was analyzed. After including all miRNAs into one multivariate Cox regression model, only miR-126 was predictive of future occurrence of long-term all-cause death (HR = 5.82, 95% CI: 1.3-24.9; p = 0.024). Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively). To conclude, miR-126 expression is a strong and independent predictor of long-term all-cause mortality among patients with T2DM. Moreover, miR-223, miR-126 and Let-7e present significant interactions with antiplatelet treatment regimens and clinical outcomes.
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