<p>Carotid artery stenosis (CAS) is the primary cause of ischemic stroke, and its pathological feature is the abnormal activation of vascular smooth muscle cells (VSMCs). Research has confirmed that miRNA plays a significant role in this pathological change. This study aims to explore the mechanism of miR-493-3p in CAS and its regulatory relationship with YTHDF2. Firstly, the association between the serum miR-493-3p levels of patients with CAS and the degree of stenosis was analyzed, and the diagnostic value was evaluated through the ROC curve. A pathological model was constructed by inducing VSMCs with Ox-LDL. The proliferation and migration abilities of the cells, as well as inflammatory factors, were detected by using the CCK-8, Transwell assay and ELISA. Dual-luciferase reporter gene assay and RNA immunoprecipitation were used to verify the targeting relationship between miR-493-3p and YTHDF2. Patients with low expression of miR-493-3p had a more severe degree of carotid artery stenosis. The sensitivity of miR-493-3p in diagnosing CAS was 90.12%, and the specificity was 86.21%. In VSMCs induced by Ox-LDL, overexpression of miR-493-3p could inhibit the proliferation, migration, and release of inflammatory factors. YTHDF2 is a direct target of miR-493-3p. Overexpression of YTHDF2 could reverse the inhibitory effect of miR-493-3p on the pathological behavior of VSMCs. miR-493-3p regulates the abnormal proliferation and migration of VSMCs by inhibiting YTHDF2. This not only provides a basis for it to be used as a diagnostic marker for CAS, but also indicates its potential as a new therapeutic target.</p>