维生素 D 缺乏促进 CVD 患者血管钙化的机制研究

为探究维生素 D 缺乏对血管钙化（vascular calcification，VC）的作用机制，文章对心血管疾病（cardiovascular disease，CVD）患者的血清学指标进行临床研究分析，发现血清维生素 D、纤维母细胞生长因子 23（fibroblast growth factor 23，FGF23）、Klotho 水平均与血管钙化相关；采用 HASMC 细胞构建钙化模型，在去除或回补维生素 D 的条件下，观察钙化相关分子在蛋白和 mRNA 水平的表达情况。结果表明，维生素 D 缺乏会引起循环系统、血管组织、肾脏组织中 Klotho 水平下降，导致 FGF23-Klotho 轴紊乱，从而产生 FGF23 抵抗，抑制 FGF23 对磷酸盐的代谢过程，导致体内磷酸盐代谢紊乱，加速血管钙化的发生发展。

In order to investigate the mechanism of vitamin D deficiency on vascular calcification(VC), this paper analyzed the serological indexes of cardiovascular disease(CVD) patients and found that serum vitamin D, fibroblast growth factor 23(FGF23) and Klotho levels were associated with VC. The HASMC cells were used to construct a calcification model, and under the condition of removing or supplementing vitamin D, calcification-related molecules were observed at the protein and mRNA levels. The results showed that vitamin D deficiency caused a decrease in Klotho levels in the circulatory system, vascular tissues, and kidney tissues, resulting in disruption of the FGF23-Klotho axis, which led to FGF23 resistance, inhibiting the metabolic process of phosphate by FGF23, leading to disruption of phosphate metabolism in vivo and accelerating the development of VC.