Evaluation of the role of FGF23 in mineral metabolism.

Hiroki Yokota, João F Raposo, Andy Chen, Chang Jiang, Hugo G Ferreira
{"title":"Evaluation of the role of FGF23 in mineral metabolism.","authors":"Hiroki Yokota,&nbsp;João F Raposo,&nbsp;Andy Chen,&nbsp;Chang Jiang,&nbsp;Hugo G Ferreira","doi":"10.4137/grsb.s2990","DOIUrl":null,"url":null,"abstract":"<p><p>Fibroblast growth factor 23 (FGF23) has recently been identified as a critical regulatory factor in phosphate (P) metabolism. Although the exact molecular mechanism of FGF23 synthesis through sensing the concentration of P is yet to be determined, experimental and clinical data indicate the influential role of FGF23 in P and calcium (Ca) homeostasis. Here, we extended our previous mathematical model in calcium regulation and examined the conceivable roles of FGF23 in mineral metabolism. We assumed that the level of FGF23 was controlled through the concentrations of P and calcitriol in serum, and its actions such as lowering of the renal threshold for P, inhibition of the production of calcitriol in the kidney tubule, and inhibition of the production of parathyroid hormone (PTH) were included. Comparisons between the models with and without FGF23 demonstrate a complex interplay of FGF23 with calcitriol and PTH. In consistent with the model, our in vitro experimentation indicates that expression of FGF23 is activated in the presence of P though a G-protein linked receptor. We expect that further efforts on modeling and experimental evaluation would contribute to diagnosing patients with metabolic diseases such as osteoporosis and chronic kidney diseases, and developing FGF23-linked treatment strategies.</p>","PeriodicalId":73138,"journal":{"name":"Gene regulation and systems biology","volume":"3 ","pages":"131-42"},"PeriodicalIF":0.0000,"publicationDate":"2009-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/grsb.s2990","citationCount":"11","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene regulation and systems biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4137/grsb.s2990","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 11

Abstract

Fibroblast growth factor 23 (FGF23) has recently been identified as a critical regulatory factor in phosphate (P) metabolism. Although the exact molecular mechanism of FGF23 synthesis through sensing the concentration of P is yet to be determined, experimental and clinical data indicate the influential role of FGF23 in P and calcium (Ca) homeostasis. Here, we extended our previous mathematical model in calcium regulation and examined the conceivable roles of FGF23 in mineral metabolism. We assumed that the level of FGF23 was controlled through the concentrations of P and calcitriol in serum, and its actions such as lowering of the renal threshold for P, inhibition of the production of calcitriol in the kidney tubule, and inhibition of the production of parathyroid hormone (PTH) were included. Comparisons between the models with and without FGF23 demonstrate a complex interplay of FGF23 with calcitriol and PTH. In consistent with the model, our in vitro experimentation indicates that expression of FGF23 is activated in the presence of P though a G-protein linked receptor. We expect that further efforts on modeling and experimental evaluation would contribute to diagnosing patients with metabolic diseases such as osteoporosis and chronic kidney diseases, and developing FGF23-linked treatment strategies.

Abstract Image

Abstract Image

Abstract Image

FGF23在矿物质代谢中的作用评价。
成纤维细胞生长因子23 (FGF23)最近被确定为磷酸盐(P)代谢的关键调节因子。虽然FGF23通过感知磷浓度合成的确切分子机制尚不清楚,但实验和临床数据表明,FGF23在磷和钙(Ca)稳态中的影响作用。在这里,我们扩展了之前钙调节的数学模型,并研究了FGF23在矿物质代谢中的可能作用。我们假设FGF23的水平是通过血清中磷和骨化三醇的浓度来控制的,其作用包括降低肾对磷的阈值,抑制肾小管中骨化三醇的产生,抑制甲状旁腺激素(PTH)的产生。与不含FGF23的模型之间的比较表明,FGF23与骨化三醇和甲状旁腺激素之间存在复杂的相互作用。与模型一致,我们的体外实验表明,在P存在时,FGF23的表达通过g蛋白连接受体被激活。我们期望进一步的建模和实验评估将有助于诊断骨质疏松症和慢性肾脏疾病等代谢性疾病患者,并制定与fgf23相关的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信