颅内动脉钙化和脑卒中及脑白质损伤等密切相关。进行颅内动脉钙化病变研究，对脑卒中防治有非常重要的意义。但颅内动脉发生钙化的机制不清楚。磷是影响血管钙化的重要因素。成纤维生长因子23（FGF23）、维生素D、甲状旁腺素和Klotho蛋白在血磷代谢调节中起重要作用，但它们在动脉钙化中的相互作用尚不完全清楚。我们课题组将在既往高血压患者颅内动脉钙化研究的基础上，进行前瞻性的随访研究，探讨磷及磷代谢调节系统在颅内动脉钙化病变发生和发展中的作用；并在血管钙化病变的动物模型中，研究血管平滑肌细胞FGF23/Klotho、维生素D受体等的表达水平与血管钙盐沉积的关系。在细胞水平利用RNA干扰技术（siRNA）降低Klotho等阳性基因表达水平以探索血管细胞成骨化改变和钙盐沉积的机制。本课题研究结果将有助于深入理解血磷代谢异常与颅内动脉钙化病变的关系及作用机制，为颅内动脉钙化的防治寻找新的干预靶点。

Intracranial arterial calcification (IAC) is closely associated with stroke and cerebral white matter lesions. Therefore, the research on IAC holds very important value for stroke prevention and therapy. However, the pathogenesis of IAC was unclear. Phosphate homeostasis is an important factor for arterial calcification. Fibroblast growth factor 23 (FGF23), vitamin D, parathyroid hormone and Klotho play very important roles in phosphate homeostasis. However, how they interact and play a role in arterial calcification is not fully understood. On the basis of our previous research on IAC in hypertensive patients, we will carry on a follow-up study to explore if phosphate and its regulators may play a causal role in the incidence and progression of IAC. In a rat model with arterial calcification, we will study the relation between arterial calcification and the expression of FGF23/Klotho, viatamin D receptor, etc in arteries. In vascular smooth muscle cells, RNA intervention of Klotho will be used to investigate the relationship between decreased expression of Klotho and vascular calcification. Our study will help in understanding the relation between abnormal phosphate homeostasis and IAC and its involved mechanisms, and may help in finding a novel intervention target for IAC.