The diagnostic and functional values of circFOXP1 in acute myocardial infarction.

BACKGROUND

Circular RNAs (circRNAs) are implicated in the pathogenesis of acute myocardial infarction (AMI). Current research aims to evaluate the diagnostic and functional value of circFOXP1 in AMI patients.

METHODS

The expression of circFOXP1 was assessed using RT-qPCR, and its diagnostic potential was determined through receiver operating characteristic (ROC) curve. The target gene of circFOXP1 was identified using a luciferase reporter assay. An in vitro hypoxia/reoxygenation (H/R) model was established in AC16 cells, while an AMI model was constructed in C57BL/6 mice. The proliferation and apoptosis of AC16 cells were evaluated using CCK8 and flow cytometry (FCM). The impact of circFOXP1 on inflammation was measured by assessing levels of TNF-α, IL-1β, and IL-6, while the effects of circFOXP1 on oxidative stress were evaluated through measurements of reactive oxygen species (ROS), glutathione (GSH), and lactate dehydrogenase (LDH) levels.

RESULTS

circFOXP1 expression was found to be downregulated in AMI patients compared to controls. The ROC curve indicated an area under the curve (AUC) was 0.881 (95%CI=0.847-0.915), with a sensitivity of 0.930 and a specificity of 0.785. Additionally, miR-9-3p was identified as a direct target gene of circFOXP1. High levels of circFOXP1 did not significantly affect f the proliferation of H/R stimulated AC16 cells; however, increased circFOXP1 resulted in significant reduction in cell apoptosis (P<0.001). TNF-α, IL-1β, and IL-6 levels were significantly lower in pcDNA3.1-circFOXP1-transfected cells (P<0.001). ROS concentration and LDH level were markedly reduced in these cells (P<0.01), while GSH level (P<0.001) was significantly elevated. miR-9-3p, as a direct target gene of circFOXP1, was found to reverse the effects of circFOXP1 on H/R AC16 cells and AMI model.

CONCLUSIONS

circFOXP1 was decreased in AMI patients and may serve as a diagnostic marker for AMI. Overexpression of circFOXP1 was shown to suppress apoptosis, inflammation, and oxidative stress via miR-9-3p in AC16 cells and the AMI model.