Regulation of Fibroblast Growth Factor 23 by Iron, EPO, and HIF.
Regulation of Fibroblast Growth Factor 23 by Iron, EPO, and HIF.
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DOI：
10.1007/s40610-019-0110-9
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发表时间：
2019-03-01
期刊：
影响因子：
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通讯作者：
Clinkenbeard, Erica L
中科院分区：
文献类型：
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作者：
Wheeler, Jonathan A;Clinkenbeard, Erica L
综述目的：成纤维细胞生长因子-23（FGF 23）是骨中产生的对磷酸盐稳态至关重要的关键激素。升高的血清磷和1，25-二羟维生素D刺激FGF 23的产生，从而促进肾磷酸盐排泄并减少1，25-二羟维生素D的合成。从而完成反馈回路并抑制FGF 23。出乎意料的是，常见和罕见的遗传性疾病的磷酸盐处理的研究确定铁和FGF 23之间的联系，证明新的监管以外的磷酸盐pathway.Recent Findings：缺铁结合FGF 23裂解突变被发现诱导常染色体显性低磷酸盐血症佝偻病表型。对铁缺乏的生理反应，如促红细胞生成素的产生以及缺氧诱导因子的激活，已经表明在调节FGF 23中。此外，特定的铁制剂，用于治疗缺铁，改变翻译后加工，从而改变FGF 23蛋白secretory.Summary：分子和临床研究表明，缺铁，通过几种机制，改变FGF 23在转录和翻译后水平。本文将重点介绍铁及其调节剂对FGF 23生物活性的影响。
PURPOSE OF REVIEW: Fibroblast growth factor-23 (FGF23) is the key hormone produced in bone critical for phosphate homeostasis. Elevated serum phosphorus and 1,25dihydroxyvitaminD stimulates FGF23 production to promote renal phosphate excretion and decrease 1,25dihydroxyvitaminD synthesis. Thus completing the feedback loop and suppressing FGF23. Unexpectedly, studies of common and rare heritable disorders of phosphate handling identified links between iron and FGF23 demonstrating novel regulation outside the phosphate pathway.RECENT FINDINGS: Iron deficiency combined with an FGF23 cleavage mutation was found to induce the autosomal dominant hypophosphatemic rickets phenotype. Physiological responses to iron deficiency, such as erythropoietin production as well as hypoxia inducible factor activation, have been indicated in regulating FGF23. Additionally, specific iron formulations, used to treat iron deficiency, alter post-translational processing thereby shifting FGF23 protein secretion.SUMMARY: Molecular and clinical studies revealed that iron deficiency, through several mechanisms, alters FGF23 at the transcriptional and post-translational level. This review will focus upon the novel discoveries elucidated between iron, its regulators, and their influence on FGF23 bioactivity.