FGF23 in skeletal modeling and remodeling.

FGF23 in skeletal modeling and remodeling.
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DOI:
10.1007/s11914-011-0053-4
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发表时间:
2011-06
影响因子:
4.3
通讯作者:
Feng, Jian Q
Feng, Jian Q
中科院分区:
医学2区
文献类型:
--
作者:
Lu, Yongbo;Feng, Jian Q

文献摘要

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成纤维细胞生长因子23 (FGF23)是一种主要由骨细胞产生的激素,它以肾脏为靶点,加速磷酸盐排泄到尿液中,抑制维生素D的合成,从而诱导负磷酸盐平衡。遗传性疾病如低磷血症性佝偻病导致血清FGF23过多导致磷酸盐浪费和骨矿化受损。相反,FGF23缺乏与高磷血症、125 (OH)2D3升高、软组织异位骨化和骨骼矿化缺陷有关。近年来对人类遗传疾病和基因工程小鼠以及体外方法的研究,揭示了FGF23调控及其在骨建模和重塑中的潜在作用,本文就这些研究进展进行综述。
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)2D3, 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.