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.