Evidence map›Paper›PMID 19669798›Full record

ReviewPediatric nephrology (Berlin, Germany)2010

Regulation of phosphate transport by fibroblast growth factor 23 (FGF23): implications for disorders of phosphate metabolism.

Jyothsna Gattineni, Michel Baum

Abstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 86 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Rickets guidance: part I-diagnostic workup.Pediatric nephrology (Berlin, Germany) · 2022
    Review
  10. Observational
  11. Article
  12. Review
  13. Article
  14. Research Models for Studying Vascular Calcification.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Jyothsna GattineniDepartment of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9063, USA.
Michel Baum
The University of Texas Southwestern Medical Center · US

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
RENAL CONTROL OF BODY COMPOSITION AND BLOOD PRESSURET32DK007257 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1986 to 2021
$5.0M
Neonatal Proximal Tubule AcidificationR01DK041612 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1991 to 2013
$2.7M
Effect of Prenatal Programming on Renal Tubular TransportR01DK078596 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD · 2009 to 2012
$1.3M
Proximal Tubule Transport Defect in Hyp MiceR01DK065842 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL G. · 2005 to 2007
$684k
NIDDK NIH HHS DK065842NIDDK NIH HHS DK078596NIDDK NIH HHS DK41612NIDDK NIH HHS P30 DK079328NIDDK NIH HHS P30DK079328NIDDK NIH HHS R01 DK041612NIDDK NIH HHS R01 DK065842NIDDK NIH HHS R01 DK078596NIDDK NIH HHS T32 DK007257NIDDK NIH HHS T32 DK07257
6 · The paper itself

Abstract

There are a number of hypophosphatemic disorders due to renal phosphate wasting that cannot be explained by elevated levels of parathyroid hormone. The circulating factors responsible for the phosphaturia have been designated as phosphatonins. Studies of patients with tumor-induced osteomalacia and other genetic diseases of phosphate metabolism have resulted in the identification of a number of hormones that regulate phosphate homeostasis, including matrix extracellular phosphoglycoprotein (MEPE), secreted frizzled-related protein 4 (sFRP-4), dentin matrix protein 1 (DMP1), fibroblast growth factor 7 (FGF7), fibroblast growth factor 23 (FGF23), and Klotho. Our understanding of the actions of these hypophosphatemic peptides has been enhanced by studies in mice either overexpressing or not expressing these hormones. This review focuses on FGF23 since its regulation is disordered in diseases that affect children, such as X-linked hypophosphatemia, autosomal dominant and recessive hypophosphatemic rickets as well as chronic kidney disease. Recent studies have shown that FGF23 is unique among the FGFs in its requirement for Klotho for receptor activation. Here, we also discuss new potentially clinically important data pointing to the receptor(s) that mediate the binding and action of FGF23 and Klotho.

Indexed as

AnimalsBiological TransportBiomarkersDisease Models, AnimalFamilial Hypophosphatemic RicketsFibroblast Growth Factor-23Fibroblast Growth FactorsGenetic Diseases, X-LinkedGlucuronidaseHumansHypophosphatemiaKidney Failure, ChronicKidney Tubules, ProximalKlotho ProteinsMiceNeoplasmsBiomarkersFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphates

Identifiers

PMID19669798
PMCPMC3151467
OpenAlexW2025339350

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.