IMPACT OF CIRCPSD3 ON ACUTE MYOCARDIAL INFARCTION PROGRESSION VIA THE MIR-338-3P/KLF6 AXIS: IMPLICATIONS FOR ATHLETIC HEALTH

Abstract

Objective: To explore the mechanism by which circPSD3 influences the progression of acute myocardial infarction (AMI) through the miR-338-3p/KLF6 axis, providing insights for interventions in athletes who are at risk or suffer from AMI. Methods: In this study, we utilized rat models and cultured cardiomyocytes to investigate the role of circPSD3. Expression levels of circPSD3, miR-338-3p, and KLF6 were analyzed using qRT-PCR and Western blot. The interaction between miR-338-3p and KLF6 was verified through dual-luciferase reporter assays. The effects of circPSD3 on cell apoptosis and infarct size were assessed using TUNEL staining and echocardiography, respectively. Results: The analysis indicated that circPSD3 levels were significantly reduced in myocardial tissues following AMI induction. Overexpression of circPSD3 in rat models led to a decrease in infarct size and cardiomyocyte apoptosis, suggesting a protective role. Mechanistically, circPSD3 acted as a sponge for miR-338-3p, thereby modulating the expression of KLF6, a known transcription factor involved in cardiac repair. Restoration of miR-338-3p reversed the protective effects of circPSD3 overexpression, highlighting the critical role of the miR-338-3p/KLF6 axis in mediating these effects. Conclusion: Our findings suggest that circPSD3 ameliorates AMI progression through modulation of the miR-338-3p/KLF6 axis. This molecular pathway may represent a novel target for therapeutic intervention, particularly for athletes exposed to high cardiac stress, potentially enhancing their cardiac resilience and recovery capabilities.