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摘要
En 中文
Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasting, inappropriately low circulating levels of the active form of vitamin 0, and skeletal abnormalities. The precise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear. In this issue of the JCI, Bai and colleagues demonstrate that deletion or inhibition of CYP24A1, which initiates degradation of the active form of vitamin D, ameliorates skeletal abnormalities in two mouse models of hypophosphatemic rickets. While this work supports an important role for excess CYP24A1 activity in the pathogenesis of FGF23-mediated hypophosphatemic rickets, more work will need to be done before CYP24A1 inhibition can be integrated into the management of patients living with these diseases.
Keyword:
X-LINKED HYPOPHOSPHATEMIA
VITAMIN-D METABOLISM
MUTATIONS
CYP24A1
FGF23
BONE
1-ALPHA,25-DIHYDROXYVITAMIN
MINERALIZATION
HYPERCALCEMIA
CALCITRIOL
期刊
IF:
13.6
论文数:
1.5W
被引数:
13.4W
机构
引用论文
Altered pharmacokinetics of 1α,25-dihydroxyvitamin D3 and 25-hydroxyvitamin D3 in the blood and tissues of the 25-hydroxyvitamin D-24-hydroxylase (Cyp24a1) null mouse.png)
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ENDOCRINOLOGYIF3.3
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