华法林与血管钙化

华法林是临床用于预防血栓栓塞的首选长效抗凝药物。然而长期低剂量或短期大剂量服用华法林会诱导冠状动脉和周围的脉管系统血管钙化，加重心房颤动患者及慢性肾病患者血管钙化程度，影响心血管功能，加重高血压等基础疾病。有研究显示槲皮素、骨保护素可以通过干预Wnt/β-catenin、TG2/β-catenin、BMP2及EPA/MMP-9等信号通路减轻华法林诱导的血管钙化，但具体作用机理尚不明确。因此，如何在保证华法林发挥抗凝效果的同时，有效降低其诱导的血管钙化是临床迫切需要解决的问题。为了进一步开展华法林发挥抗凝效果的同时降低其诱导的血管钙化的相关研究，本文从华法林诱导血管钙化的临床现象、分子机制及潜在预防华法林诱导血管钙化的药物等方面进行综述，为合理使用华法林抗凝，降低其诱导血管钙化提供参考。

Warfarin and vascular calcification

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.