Abstract: Warfarin is the first choice long-acting anticoagulant drug for clinical prevention of thromboembolism. However, long-term low-dose or short-term high-dose administration of warfarin can induce vascular calcification, mainly including the induction of vascular calcification in the coronary arteries and surrounding vasculature. It can induce vascular calcification in patients with atrial fibrillation and patients with chronic kidney disease, affect cardiac functions, and aggravate underlying diseases such as hypertension. Studies have shown that quercetin and osteoprotegerin could reduce warfarin-induced vascular calcification by interfering with Wnt/β-catenin, TG2/β-catenin, BMP2 and EPA/MMP-9 signaling pathways, but the specific action mechanism is not yet clear. Therefore, how to effectively reduce the induced vascular calcification and at the same time ensure the anticoagulant effect of warfarin is an urgent clinical problem to be solved. This article will review the clinical phenomena, molecular mechanisms, and potential prevention of warfarin-induced vascular calcification in warfarin-induced vascular calcification and provide a reference for the rational use of warfarin anticoagulation to reduce its induced vascular calcification.