FGF23 Synthesis and Activity.

Current molecular biology reports Pub Date : 2019-03-01 Epub Date: 2019-01-17 DOI:10.1007/s40610-019-0111-8
Megan L Noonan, Kenneth E White
{"title":"FGF23 Synthesis and Activity.","authors":"Megan L Noonan, Kenneth E White","doi":"10.1007/s40610-019-0111-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>The phosphaturic hormone FGF23 is produced primarily in osteoblasts/osteocytes and is known to respond to increases in serum phosphate and 1,25(OH)<sub>2</sub> vitamin D (1,25D). Novel regulators of FGF23 were recently identified, and may help explain the pathophysiologies of several diseases. This review will focus on recent studies examining the synthesis and actions of FGF23.</p><p><strong>Recent findings: </strong>The synthesis of FGF23 in response to 1,25D is similar to other steroid hormone targets, but the cellular responses to phosphate remain largely unknown. The activity of intracellular processing genes control FGF23 glycosylation and phosphorylation, providing critical functions in determining the serum levels of bioactive FGF23. The actions of FGF23 largely occur through its co-receptor αKlotho (KL) under normal circumstances, but FGF23 has KL-independent activity during situations of high concentrations.</p><p><strong>Summary: </strong>Recent work regarding FGF23 synthesis and bioactivity, as well as considerations for diseases of altered phosphate balance will be reviewed.</p>","PeriodicalId":72737,"journal":{"name":"Current molecular biology reports","volume":"5 1","pages":"18-25"},"PeriodicalIF":0.0000,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469709/pdf/nihms-1524962.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current molecular biology reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s40610-019-0111-8","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2019/1/17 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Purpose of review: The phosphaturic hormone FGF23 is produced primarily in osteoblasts/osteocytes and is known to respond to increases in serum phosphate and 1,25(OH)2 vitamin D (1,25D). Novel regulators of FGF23 were recently identified, and may help explain the pathophysiologies of several diseases. This review will focus on recent studies examining the synthesis and actions of FGF23.

Recent findings: The synthesis of FGF23 in response to 1,25D is similar to other steroid hormone targets, but the cellular responses to phosphate remain largely unknown. The activity of intracellular processing genes control FGF23 glycosylation and phosphorylation, providing critical functions in determining the serum levels of bioactive FGF23. The actions of FGF23 largely occur through its co-receptor αKlotho (KL) under normal circumstances, but FGF23 has KL-independent activity during situations of high concentrations.

Summary: Recent work regarding FGF23 synthesis and bioactivity, as well as considerations for diseases of altered phosphate balance will be reviewed.

FGF23 的合成与活性。
综述目的:磷酸化激素 FGF23 主要在成骨细胞/骨细胞中产生,已知会对血清磷酸盐和 1,25(OH)2 维生素 D(1,25D)的增加做出反应。最近发现了 FGF23 的新型调节因子,它们可能有助于解释多种疾病的病理生理。本综述将重点介绍最近对 FGF23 的合成和作用进行的研究:FGF23对1,25D的合成反应与其他类固醇激素靶点相似,但细胞对磷酸盐的反应在很大程度上仍然未知。细胞内加工基因的活性控制着 FGF23 的糖基化和磷酸化,在决定血清中生物活性 FGF23 水平方面发挥着关键作用。在正常情况下,FGF23的作用主要通过其共同受体αKlotho(KL)来实现,但在高浓度情况下,FGF23具有不依赖于KL的活性:将对有关 FGF23 合成和生物活性的最新研究成果以及对磷酸盐平衡改变的疾病的考虑进行综述。
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