近年研究认为Wnt信号不但调控肿瘤和发育，也调节成人血管损伤的病理过程，但慢性肾病的血管钙化是否受其调节未知。本研究旨在探讨Wnt/beta-Catenin信号调节慢性肾病的血管平滑肌细胞钙化的分子机制。我们的前期工作发现Wnt1通过激活beta-Catenin信号上调钙化抑制因子焦磷酸(PPi)水平而抑制血管钙化。据此提出假说Wnt/beta-Catenin调节PPi是血管钙化的病理机制之一。本项目首次探讨Wnt/beta-Catenin通过PPi调节血管钙化的分子机制，研究内容包括：1，分析细胞水平及慢性肾衰动物模型的Wnt1及PPi变化的关系；2，研究Wnt1对血管钙化以及PPi调节的分子机制；3，探讨Wnt1上调PPi在血管钙化在细胞及动物模型中的作用。本研究对深入认识血管钙化病理过程中Wnt1的作用以及PPi的调控机制具有重要意义，并为临床防治慢性肾病致血管钙化提供新的靶点和思路

Recent research indicated that Wnt signal has an important role in vascular disease, in stead of oncology and embryonic development, however the mechanism of vascular calcification in chronic kidney disease was not clear. This project aimed to investigate the mechanism by which the Wnt/beta-catenin signal regulates the calcification of human vascular smooth muscle cell. Our early works has demonstrated Wnt1 can increase PPi level and inhibit the extracellular calcification.Our hypothesis is that lower Wnt1 signal and PPi level are the dependent mediator of vascular calcification. This project included:(1)Analysis the relationship between Wnt1 and PPi level in cellular and animal model; (2)Investigate the regulation mechanism of vascular calcification and PPi by Wnt1; (3)Explore the in vitro and in vivo role of Wnt1 enhancing PPi in vascular calcification. This project has important theoretical and clinical significance in prevention and cure of vascular calcification.