维生素D缺乏促进CVD患者血管钙化的机制研究  

An investigation into the mechanism by which vitamin D deficiency promotes vascular calcification in CVD patients

作　　者：朱欣然 张爽 段亚君 ZHU Xinran;ZHANG Shuang;DUAN Yajun(School of Food and Biological Engineering,Hefei University of Technology,Hefei 230601,China)

机构地区：[1]合肥工业大学食品与生物工程学院,安徽合肥230601

出　　处：《合肥工业大学学报(自然科学版)》2025年第1期112-118,126,共8页Journal of Hefei University of Technology:Natural Science

基　　金：国家自然科学基金资助项目(82173807);中央高校基本科研业务费专项资金资助项目(JZ2021HGTA0127)。

摘　　要：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.

关 键 词：维生素D FGF23-Klotho轴 血管钙化(VC) 心血管疾病(CVD) FGF23抵抗 

分 类 号：R977.24[医药卫生—药品]