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2
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本文引用的文献

1
FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis.成纤维细胞生长因子23是维生素D代谢和磷酸盐稳态的有效调节因子。
J Bone Miner Res. 2004 Mar;19(3):429-35. doi: 10.1359/JBMR.0301264. Epub 2003 Dec 29.
2
FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting.骨纤维异常增殖症中的成纤维细胞生长因子-23及其与肾性磷酸盐消耗的关系。
J Clin Invest. 2003 Sep;112(5):683-92. doi: 10.1172/JCI18399.
3
Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia.成骨细胞骨软化症和X连锁低磷血症中的成纤维细胞生长因子23
N Engl J Med. 2003 Apr 24;348(17):1656-63. doi: 10.1056/NEJMoa020881.
4
The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency.成纤维细胞生长因子23中的常染色体显性低磷血症佝偻病R176Q突变可抵抗蛋白水解切割并增强体内生物学活性。
J Biol Chem. 2003 Mar 14;278(11):9843-9. doi: 10.1074/jbc.M210490200. Epub 2003 Jan 7.
5
Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia.低磷性佝偻病/骨软化症患者体内具有生物活性的全长成纤维细胞生长因子23（FGF-23）循环水平升高。
J Clin Endocrinol Metab. 2002 Nov;87(11):4957-60. doi: 10.1210/jc.2002-021105.
6
Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo.导致常染色体显性低磷性佝偻病的突变型成纤维细胞生长因子23（FGF-23）对蛋白水解切割具有抗性，并在体内导致低磷血症。
Endocrinology. 2002 Aug;143(8):3179-82. doi: 10.1210/endo.143.8.8795.
7
Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23.常染色体显性低磷性佝偻病（ADHR）突变使成纤维细胞生长因子23（FGF-23）稳定。
Kidney Int. 2001 Dec;60(6):2079-86. doi: 10.1046/j.1523-1755.2001.00064.x.
8
Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia.成纤维细胞生长因子23作为肿瘤诱导性骨软化症致病因素的克隆与鉴定
Proc Natl Acad Sci U S A. 2001 May 22;98(11):6500-5. doi: 10.1073/pnas.101545198. Epub 2001 May 8.
9
The autosomal dominant hypophosphatemic rickets (ADHR) gene is a secreted polypeptide overexpressed by tumors that cause phosphate wasting.常染色体显性遗传性低磷血症性佝偻病（ADHR）基因是一种由导致磷酸盐消耗的肿瘤过度表达的分泌型多肽。
J Clin Endocrinol Metab. 2001 Feb;86(2):497-500. doi: 10.1210/jcem.86.2.7408.
10
Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23.常染色体显性低磷性佝偻病与FGF23基因突变有关。
Nat Genet. 2000 Nov;26(3):345-8. doi: 10.1038/81664.

对Fgf23进行靶向消融表明FGF23在磷酸盐和维生素D代谢中具有重要的生理作用。

Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism.

作者信息

Shimada Takashi, Kakitani Makoto, Yamazaki Yuji, Hasegawa Hisashi, Takeuchi Yasuhiro, Fujita Toshiro, Fukumoto Seiji, Tomizuka Kazuma, Yamashita Takeyoshi

机构信息

Pharmaceutical Research Laboratories, KIRIN Brewery Co., Takasaki, Gunma, Japan.

出版信息

J Clin Invest. 2004 Feb;113(4):561-8. doi: 10.1172/JCI19081.

DOI:10.1172/JCI19081
PMID:14966565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC338262/
Abstract

Inorganic phosphate is essential for ECM mineralization and also as a constituent of important molecules in cellular metabolism. Investigations of several hypophosphatemic diseases indicated that a hormone-like molecule probably regulates serum phosphate concentration. FGF23 has recently been recognized as playing important pathophysiological roles in several hypophosphatemic diseases. We present here the evidence that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF23-null mice. Disruption of the Fgf23 gene did not result in embryonic lethality, although homozygous mice showed severe growth retardation with abnormal bone phenotype and markedly short life span. The Fgf23(-/-) mice displayed significantly high serum phosphate with increased renal phosphate reabsorption. They also showed an elevation in serum 1,25(OH)2D that was due to the enhanced expression of renal 25-hydroxyvitamin D-1alpha-hydroxylase (1alpha-OHase) from 10 days of age. These phenotypes could not be explained by currently known regulators of mineral homeostasis, indicating that FGF23 is essential for normal phosphate and vitamin D metabolism.

摘要

无机磷酸盐对于细胞外基质矿化至关重要，也是细胞代谢中重要分子的组成成分。对几种低磷血症疾病的研究表明，一种类似激素的分子可能调节血清磷酸盐浓度。成纤维细胞生长因子23（FGF23）最近被认为在几种低磷血症疾病中发挥重要的病理生理作用。我们在此通过构建FGF23基因敲除小鼠，提供证据表明FGF23是血清磷酸盐和1,25-二羟维生素D（1,25[OH]2D）的生理调节因子。尽管纯合小鼠表现出严重的生长迟缓和异常的骨骼表型以及明显缩短的寿命，但Fgf23基因的破坏并未导致胚胎致死。Fgf23（-/-）小鼠血清磷酸盐显著升高，肾磷酸盐重吸收增加。它们还表现出血清1,25（OH）2D升高，这是由于从10日龄起肾25-羟维生素D-1α-羟化酶（1α-OHase）表达增强所致。这些表型无法用目前已知的矿物质稳态调节因子来解释，表明FGF23对于正常的磷酸盐和维生素D代谢至关重要。