Clinical significance of miR-218-5p and its potential mechanism in acute pulmonary embolism.

INTRODUCTION AND

OBJECTIVE

Acute pulmonary embolism (APE), a life-endangering cardiovascular acute disorder, brings about difficulties in early diagnosis. The aim of the study is to investigate the expression of miR-218-5p, its clinical significance, and mechanism in APE.

MATERIAL AND

METHODS

A total of 102 APE patients and 98 healthy controls were recruited, with miR-218-5p levels assayed by qRT-PCR; its diagnostic value was assessed by ROC curves. Pearson correlation and multivariate logistic regression analyzed associations with clinical indicators and independent predictive value. Oxygen-glucose deprivation/reoxygenation (OGD/R)-induced human pulmonary artery endothelial cells (HPAECs) were transfected with miR-218-5p mimic to observe the effects on apoptosis, proliferation, inflammation, and oxidative stress. Bioinformatics and dual-luciferase assays validated miR-218-5p targeting CREB1.

RESULTS

Serum miR-218-5p was significantly downregulated in APE (P<0.0001) with high diagnostic efficacy (AUC=0.893). It positively correlated with D-dimer (r=0.759) and Wells scores (r=0.703; P<0.0001) and was an independent APE risk factor (OR=0.053; P<0.0001). In vitro, miR-218-5p overexpression reduced OGD/R-induced HPAEC apoptosis, promoted proliferation, inhibited inflammation (IL-6, IL-1β, TNF-α) and oxidative stress (MDA, ROS), and restored SOD activity (P<0.01). Mechanistically, miR-218-5p directly targeted CREB1 to suppress its expression.

CONCLUSIONS

miR-218-5p is downregulated in APE, as a potential diagnostic biomarker. It targets CREB1 to modulate apoptosis, inflammation, and oxidative stress, thereby contributing to APE pathogenesis.