Optimizing Cardiac Health in Athletes: Analyzing the Role of miR-155 Antagonist in Regulating Th17/Treg Pathways and Mitigating Myocardial Fibrosis in Myocarditis

Abstract

Purpose: This study investigates the role of a miR-155 antagonist in regulating the Th17/Treg signaling pathway and its effects on myocardial fibrosis in myocarditis, with a focus on potential applications for athlete health management. Method: An autoimmune myocarditis model was established in BALB/C mice through cardiac myosin immunization (n=30), subdivided into four groups: model group (MG, n=10, phosphate buffer solution injected), inhibitor group (IG, n=10, miR-155 antagonist injected), negative control group (NCG, n=10, injected with a non-sense random sequence), and a healthy control group (CG, n=10, phosphate buffer solution injected). Differences in miR-155 expression were measured among the groups alongside IL-17 and TGF-β levels in myocardial tissue by RT-PCR and ELISA. Results: The miR-155 expression was significantly lower in the inhibitor group compared to the model and negative control groups (P<0.05), indicating effective inhibition. Correspondingly, IL-17 and TGF-β mRNA levels were significantly reduced in the inhibitor group (P<0.05), suggesting a decrease in inflammatory and fibrotic markers. The inhibitor group exhibited marked reductions in IL-17 and TGF-β expression on day 21 compared to other groups, underscoring the potential therapeutic benefits of miR-155 inhibition in reducing myocardial fibrosis. Conclusion: The inhibition of miR-155 significantly curtails the progression of myocardial fibrosis in myocarditis by modulating the Th17/Treg signaling pathway. This mechanism may offer valuable insights for developing strategies to manage cardiovascular health in athletes, particularly those recovering from or susceptible to myocarditis, enhancing their overall cardiac function and performance sustainability.