Evidence map›Paper›PMID 31218207›Full record

ArticleCurrent molecular biology reports2019

Regulation of Fibroblast Growth Factor 23 by Iron, EPO, and HIF.

Jonathan A Wheeler, Erica L Clinkenbeard

Abstract read
In one paragraph

Article in Current molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. FGF23 - A hormone produced by bone and has many faces.Reviews in endocrine & metabolic disorders · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The regulation of FGF23 under physiological and pathophysiological conditions.Pflugers Archiv : European journal of physiology · 2022
    Review
  18. Roles of osteocytes in phosphate metabolism.Frontiers in endocrinology · 2022
    Review
  19. Regulation of FGF23: Beyond Bone.Current osteoporosis reports · 2021
    Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Jonathan A WheelerDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Erica L ClinkenbeardDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Comprehensive Training Program in Musculoskeletal ResearchT32AR065971 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ALEXANDER G ROBLING · 2015 to 2026
$4.4M
Role of iron and hypoxia sensing in FGF23-dependent metabolic bone diseaseF32AR065389 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI CLINKENBEARD, ERICA L · 2014 to 2016
$183k
NIAMS NIH HHS F32 AR065389NIAMS NIH HHS T32 AR065971
6 · The paper itself

Abstract

purpose of reviewFibroblast 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

findingsIron 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.

Indexed as

erythropoietinFGF-23hypoxia-inducible factorironphosphate

Identifiers

PMID31218207
PMCPMC6582956
OpenAlexW2913353125

What OpenQuestion holds

Textmetadata
LicenceTDM
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.