Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions

被引:56
作者
Agoro, Rafiou [1 ]
White, Kenneth E. E. [1 ,2 ]
机构
[1] Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA
[2] Indiana Univ, Sch Med, Dept Med, Div Nephrol, Indianapolis, IN 46202 USA
关键词
FIBROBLAST GROWTH FACTOR-23; DOMINANT HYPOPHOSPHATEMIC RICKETS; PARATHYROID-HORMONE; DISEASE PROGRESSION; ALPHA-KLOTHO; GENE LEADS; EXPRESSION; FIBROBLAST-GROWTH-FACTOR-23; HYPERPHOSPHATEMIA; DEFICIENCY;
D O I
10.1038/s41581-022-00665-x
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The bone-derived hormone fibroblast growth factor 23 (FGF23) functions in concert with parathyroid hormone (PTH) and the active vitamin D metabolite, 1,25(OH)(2) vitamin D (1,25D), to control phosphate and calcium homeostasis. A rise in circulating levels of phosphate and 1,25D leads to FGF23 production in bone. Circulating FGF23 acts on the kidney by binding to FGF receptors and the co-receptor alpha-Klotho to promote phosphaturia and reduce circulating 1,25D levels. Various other biomolecules that are produced by the kidney, including lipocalin-2, glycerol 3-phosphate, 1-acyl lysophosphatidic acid and erythropoietin, are involved in the regulation of mineral metabolism via effects on FGF23 synthesis in bone. Understanding of the molecular mechanisms that control FGF23 synthesis in the bone and its bioactivity in the kidney has led to the identification of potential targets for novel interventions. Emerging approaches to target aberrant phosphate metabolism include small molecule inhibitors that directly bind FGF23 and prevent its interactions with FGF receptors and alpha-Klotho, FGF23 peptide fragments that act as competitive inhibitors of intact FGF23 and small molecule inhibitors of kidney sodium-phosphate cotransporters.
引用
收藏
页码:185 / 193
页数:9
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