FGF23 in skeletal modeling and remodeling

被引:38
|
作者
Lu Y. [1 ]
Feng J.Q. [1 ]
机构
[1] Department of Biomedical Sciences, Baylor College of Dentistry, Texas A and M University Health Science Center, Dallas, TX 75246
基金
美国国家卫生研究院;
关键词
DMP1; FGF23; Hyp; Hypophosphatemic rickets; Modeling and remodeling; Phosphate homeostasis;
D O I
10.1007/s11914-011-0053-4
中图分类号
学科分类号
摘要
Fibroblast growth factor 23 (FGF23), a hormone primarily produced in bone cells, targets the kidney to accelerate phosphate excretion into the urine and suppresses vitamin D synthesis, thereby inducing a negative phosphate balance. Excessive serum FGF23 due to hereditary disorders such as hypophosphatemic rickets leads to phosphate wasting and impaired bone mineralization. In contrast, deficiencies in FGF23 are associated with hyperphosphatemia, elevated 1,25(OH) 2D 3, ectopic ossification in soft tissues, and defects in skeletal mineralization. Recent studies of human genetic disorders and genetically engineered mice, as well as the in vitro approaches, have clarified some mysteries in FGF23 regulation and its potential roles in bone modeling and remodeling, which are summarized in this review article. © 2011 Springer Science+Business Media, LLC.
引用
收藏
页码:103 / 108
页数:5
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