The PTH-Vitamin D-FGF23 axis

被引：133

作者：

Blau, Jenny E. ^{[1
]}

Collins, Michael T. ^{[2
]}

机构：

[1] NICHD, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA

[2] NIDCR, Skeletal Clin Studies Unit, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA

来源：

REVIEWS IN ENDOCRINE & METABOLIC DISORDERS | 2015年 / 16卷 / 02期

基金：

美国国家卫生研究院;

关键词：

Fibroblast growth factor 23 (FGF23); Parathyroid Hormone (PTH); Vitamin D; Phosphate; Hypophosphatemic rickets; Chronic Renal Failure; 1-alpha hydroxylase; FIBROBLAST-GROWTH-FACTOR; CHRONIC KIDNEY-DISEASE; X-LINKED HYPOPHOSPHATEMIA; TUMOR-INDUCED OSTEOMALACIA; RENAL PHOSPHATE-TRANSPORT; AUTOSOMAL RECESSIVE HYPOPHOSPHATEMIA; LEFT-VENTRICULAR HYPERTROPHY; 23; IN-VIVO; PARATHYROID-HORMONE; PRIMARY HYPERPARATHYROIDISM;

D O I：

10.1007/s11154-015-9318-z

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Fibroblast growth factor 23 (FGF23) has emerged as an important regulator of phosphate and vitamin D homeostasis. It is important to understand how FGF23 interacts with vitamin D and parathyroid hormone (PTH) in a FGF23-Vitamin D-PTH axis to regulate mineral homeostasis. In this review, we discuss the genomic structure, and transcriptional, translational, and posttranslational regulation of FGF23. We describe its interaction with PTH and vitamin D, disorders of altered FGF23 states, and emerging therapies for diseases of FGF23 based upon these findings. This discussion helps redefine the role of PTH and vitamin D in relation to a complex bone-kidney-parathyroid loop, and points to areas within this complicated field in need of further clarification and research.

引用

页码：165 / 174

页数：10

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