To construct a more bionic vascular calcification model of uremia. The changes of Fut8 in the vascular calcification model were determined. To explore the mechanism of miR-34c-5p on vascular calcification. Cells co-cultrue, Bioinformatics, Western and Lectin blotting, Quantitative real-time PCR analysis, Immunocytochemical staining, Luciferase reporter assay, Lectin pull-down assay, Alizarin red staining, Measurement of Fut8 activity, Calcium content assays. In endothelial/smooth muscle cell co-culture systems, overexpressed miR-34c-5p promoted uremia serum-induced calcification in HASMCs(Fig1). Fut8 was increased in calcification model(Fig1). miR-34c-5p targeted Fut8 and negatively regulate the calcification(Fig1). In our previous study, inhibition of Fut8 mitigated vascular calcification. Overexpression miR-34c-5p affects expression of Fut8 and suppresses uremic serum-induced HASMCs calcification. Oe-Fut8 effectively reverses the expression of miR-34-5p in vitro. (Fig2). In uremic vascular calcification disease, miR-34c-5p can down-regulate the degree of calcification by inhibiting Fut8.