Clinical Value and Potential Molecular Mechanism of miR-373-3p in Coronary Atherosclerosis.

Abstract

BackgroundCoronary atherosclerosis (CAS) is a chronic inflammatory condition marked by damage to the coronary artery endothelium, lipid accumulation, and fibrosis. It stands as the principal etiology of coronary heart disease (CHD).AimsThe rationale of this study was to investigate the clinical value and potential mechanism of miR-373-3p in carotid CAS.MethodsA total of 95 patients with CAS and 35 controls were enrolled in the study. RT-qPCR was used to evaluate the relative expression of miR-373-3p. ROC curve was used to analyze the diagnostic value of miR-373-3p in CAS. Logistic regression analysis was utilized to evaluate whether miR-373-3p serves as a risk factor for CAS. In addition, miR-373-3p overexpression and knockdown models of endothelial progenitor (EPCs) were established to investigate the mechanism of miR-373-3p in the regulation of EPCs.ResultsThe level of miR-373-3p in CAS patients was significantly increased. MiR-373-3p can well distinguish patients with CAS and is a risk factor for CAS. The over-expression of miR-373-3p can substantially inhibit the proliferation, migration and invasion of EPCs, and stimulate the apoptosis of EPCs. MiR-373-3p is involved in the progression of CAS by targeting VEGFA.ConclusionsAs a highly sensitive potential biomarker, miR-373-3p can predict the occurrence and progression of CAS. Additionally, miR-373-3p is involved in the progression of CAS by targeting VEGFA, which may play an essential role in the pathogenesis of CAS.