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慢性肾脏疾病(chronic kidney disease,CKD)普遍存在维生素D(VitD)代谢异常。活性VitD替代治疗是预防心血管并发症(cardiovascular complications,CVC)的常规方法。然而,临床研究和动物实验均显示VitD存在心血管双向调控效应,即小剂量抑制CVC,而大剂量则促进CVC的发生。其中机制尚不清楚。成纤维细胞生长因子23(fibro blast growth factor-23,FGF-23)是FGF家族新成员,在维持肾磷与VitD自稳态平衡方面发挥重要作用。VitD在促进FGF-23分泌的同时,其生物学效应又受到FGF-23的负反馈抑制。因此,FGF-23可能为阐明VitD心血管双向调控
Chronic kidney disease (CKD) prevalence of vitamin D (VitD) metabolic abnormalities. Active vitamin D replacement therapy is a common method of preventing cardiovascular complications (CVC). However, both clinical studies and animal experiments show that there is a cardiovascular bi-directional regulation effect on VitD, that is, CVC is inhibited by a small dose, while CVC is promoted by a large dose. The mechanism is not clear. Fibroblast growth factor-23 (FGF-23), a new member of the FGF family, plays an important role in maintaining homeostasis balance between renal and P vitD. VitD, in addition to promoting FGF-23 secretion, is biologically negatively repressed by FGF-23. Therefore, FGF-23 may shed light on the cardiovascular regulation of VitD