Diagnostic Value and Regulatory Mechanism of miR-322-5p in Coronary Heart Disease.

Abstract

Background: Coronary heart disease (CHD) is a heart condition caused by narrowed or blocked coronary arteries. The miR-322-5p is closely related to inflammation and vascular diseases, yet its role in CHD remains unknown.

Objective: This study focused on investigating the clinical significance of miR-322-5p and its regulatory mechanism in CHD.

Materials and methods: This study enrolled 160 CHD patients and 130 healthy individuals. The expression of miR-322-5p and TRAF6 was measured by RT-qPCR. The correlation between miR-322-5p and CHD was evaluated via Pearson correlation analysis. The clinical predictive performance of miR-322-5p was assessed by ROC analysis. Cell viability was assessed using the CCK-8 assay while apoptosis was analyzed by flow cytometry. Inflammatory cytokine levels were determined by ELISA.

Results: MiR-322-5p was significantly downregulated in patients with CHD and exhibited high diagnostic accuracy for CHD with an AUC of 0.882. The declined miR-322-5p was negatively correlated with Gensini score (r = -0.611) and CRP (r = -0.646), but positively associated with HDL-C (r = 0.598). Although miR-322-5p was reduced under pathological conditions, its upregulation enhanced cell viability and inhibited both apoptosis and inflammatory factors. TRAF6, a direct target of miR-322-5p, was negatively regulated by miR-322-5p (r = -0.683), and high levels of TRAF6 aggravated CHD.

Conclusion: The declined miR-322-5p in CHD presented high diagnostic value. Reduced miR-322-5p exacerbated the CHD by inhibiting cell viability, enhancing apoptosis and inflammation through negatively regulating the TRAF6.