Fibroblast growth factor 23: state of the field and future directions

被引：110

作者：

Bhattacharyya, Nisan ^{[1
]}

Chong, William H. ^{[1
]}

Gafni, Rachel I. ^{[1
]}

Collins, Michael T. ^{[1
]}

机构：

[1] Natl Inst Dent & Craniofacial Res, Skeletal Clin Studies Unit, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2012年 / 23卷 / 12期

基金：

美国国家卫生研究院;

关键词：

TUMOR-INDUCED OSTEOMALACIA; CHRONIC KIDNEY-DISEASE; VITAMIN-D METABOLISM; HYPEROSTOSIS-HYPERPHOSPHATEMIA SYNDROME; AUTOSOMAL RECESSIVE HYPOPHOSPHATEMIA; HOMOZYGOUS MISSENSE MUTATION; X-LINKED HYPOPHOSPHATEMIA; RENAL PHOSPHATE-TRANSPORT; MCCUNE-ALBRIGHT-SYNDROME; PARATHYROID-HORMONE;

D O I：

10.1016/j.tem.2012.07.002

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) is a bone-derived hormone that regulates and is regulated by blood levels of phosphate and active vitamin D. Post-translational glycosylation by the enzyme GALNT3 and subsequent processing by furin have been demonstrated to be a regulated process that plays a role in regulating FGF23 levels. In physiologic states, FGF23 signaling is mediated by an FGF receptor and the coreceptor, Klotho. Recent work identifying a role for iron/hypoxia pathways in FGF23 physiology and their implications are discussed. Beyond its importance in primary disorders of mineral metabolism, recent work implicates FGF23 in renal disease-associated morbidity, as well as possible roles in cardiovascular disease and skeletal fragility.

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收藏

页码：610 / 618

页数：9

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