<scp>MiR</scp> ‐490‐3p/ <scp>TGFBR1</scp> Axis Prevents Atrial Fibrillation by Inhibiting Cellular Fibrosis

Atrial fibrillation (AF) ranks among the most prevalent cardiovascular diseases, and its prevalence is increasing over the years. Atrial fibrosis is one of the key causes of AF. This study aimed to investigate miR-490-3p levels in AF and the regulatory effect of the miR-490-3p/TGFBR1 axis on atrial fibrosis. In this study, RT-qPCR was utilized to detect miR-490-3p and TGFBR1 levels in AF patients. ROC was utilized to assess the diagnostic value of miR-490-3p in AF. Logistic regression was utilized to analyze left atrial fibrosis risk factors in AF patients. The AF cell model was established using human cardiac fibroblasts (HCFs). In vitro experiments included CCK-8 viability assay and luciferase reporter assay. The levels of fibrotic factors were detected using western blot. miR-490-3p expression in AF patients was clearly lower. miR-490-3p had good diagnostic ability for AF and was a risk factor. Luciferase assays confirmed TGFBR1 as a target of miR-490-3p. In vitro cell experiments confirmed that TGFBR1 overexpression can rescue the inhibitory effect of miR-490-3p on HCFs proliferation and fibrotic factor expression. In conclusion, miR-490-3p may act as a potential AF marker and inhibit the occurrence of atrial fibrosis through the miR-490-3p/TGFBR1 axis.