Evidence map›Paper›PMID 25792238›Full record

ArticleJournal of bone and mineral metabolism2016

Phosphate enhances Fgf23 expression through reactive oxygen species in UMR-106 cells.

Michiko Hori, Yuka Kinoshita, Manabu Taguchi, Seiji Fukumoto

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bone and mineral metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Celastrol Attenuates FGF23 Expression in Osteoblasts by Inhibiting STAT3 Activation.Endocrine, metabolic & immune disorders drug targets · 2026
    Article
  2. TGFβ signaling regulates the response of the skeleton to phosphate.bioRxiv : the preprint server for biology · 2025
    Article
  3. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
    Review
  4. A role for sirtuin 1 in FGF23 activation following β-glycerophosphate treatment.Pflugers Archiv : European journal of physiology · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. The regulation of FGF23 under physiological and pathophysiological conditions.Pflugers Archiv : European journal of physiology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Upstream Regulators of Fibroblast Growth Factor 23.Frontiers in endocrinology · 2021
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Michiko HoriDivision of Nephrology and Endocrinology, Department of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Yuka KinoshitaDivision of Nephrology and Endocrinology, Department of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Manabu TaguchiDivision of Nephrology and Endocrinology, Department of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Seiji FukumotoDivision of Nephrology and Endocrinology, Department of Medicine, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. fukumoto-tky@umin.ac.jp.
University of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 23 (FGF23) has been shown to work as a phosphotropic hormone. Although FGF23 reduces the serum phosphate level, it has not been established that phosphate directly regulates FGF23 production. In this study, we investigated whether phosphate can enhance Fgf23 expression using the rat osteoblastic cell line UMR-106, which has been shown to express Fgf23 in response to 1,25-dihydroxyvitamin D [1,25(OH)2D]. Phosphate increased Fgf23 expression in a dose- and time-dependent manner in the presence of 1,25(OH)2D. Phosphate also increased Fgf23 promoter activity, but showed no effect on the half-life of Fgf23 messenger RNA. Phosphonoformic acid and PD98059, an inhibitor of MEK, inhibited the effects of phosphate on Fgf23 expression and promoter activity. In addition, phosphate enhanced production of reactive oxygen species (ROS) in UMR-106 cells, and hydrogen peroxide enhanced FGF23 production in a dose- and time-dependent manner. Hydrogen peroxide also enhanced Elk1 reporter activity, a target of the MEK-extracellular-signal-regulated kinase (ERK) pathway. Furthermore, the effect of phosphate on ROS production and Fgf23 expression was inhibited by apocynin, an inhibitor of NADPH oxidase. These results indicate that phosphate directly enhances Fgf23 transcription without affecting the stability of Fgf23 messenger RNA by stimulating NADPH-induced ROS production and the MEK-ERK pathway in UMR-106 cells.

Indexed as

AnimalsCell LineExtracellular Signal-Regulated MAP KinasesFibroblast Growth Factor-23Fibroblast Growth FactorsGene Expression RegulationHydrogen PeroxidePhosphatesRatsReactive Oxygen SpeciesRNA, MessengerVitamin D1,25-dihydroxyvitamin DExtracellular Signal-Regulated MAP KinasesFibroblast Growth Factor-23Fibroblast Growth FactorsHydrogen PeroxidePhosphatesReactive Oxygen SpeciesRNA, MessengerVitamin D1,25-Dihydroxyvitamin DExtracellular-signal-regulated kinaseFibroblast growth factor 23PhosphateReactive oxygen species

Identifiers

PMID25792238
OpenAlexW2008282188

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.