Evidence map›Paper›PMID 28159712›Full record

ReviewBone2017

Heritable and acquired disorders of phosphate metabolism: Etiologies involving FGF23 and current therapeutics.

Erica L Clinkenbeard, Kenneth E White

Open access · greenAbstract readReview
In one paragraph

Review in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 31 citations in OpenAlex.

  1. Erythropoietin stimulates fibroblast growth factor 23 (FGF23) in mice and men.Pflugers Archiv : European journal of physiology · 2018
    Trial
  2. Article
  3. Article
  4. Approach to Hypophosphatemic Rickets.The Journal of clinical endocrinology and metabolism · 2022
    Article
  5. FGF23 signalling and physiology.Journal of molecular endocrinology · 2021
    Review
  6. Review
  7. The Causes of Hypo- and Hyperphosphatemia in Humans.Calcified tissue international · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Two Cases of Iron-Induced Hypophosphatemia.AACE endocrinology and diabetes
    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 2 institutions in 1 country.

Erica L ClinkenbeardDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Kenneth E WhiteDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: kenewhit@iupui.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

FGF-23 REGULATION OF PHOSPHATE HOMEOSTASISR01DK063934 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI WHITE, KENNETH E · 2003 to 2015
$3.8M
Control of FGF23 Bioactivity via Circulating alpha-KlothoR01DK095784 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI WHITE, KENNETH E · 2013 to 2017
$1.7M
Novel mediators of FGF23 bioactivityR21AR070329 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI WHITE, KENNETH E · 2016 to 2017
$381k
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 R21 AR070329NIDDK NIH HHS R01 DK063934NIDDK NIH HHS R01 DK095784
6 · The paper itself

Abstract

Phosphate is critical for many cellular processes and structural functions, including as a key molecule for nucleic acid synthesis and energy metabolism, as well as hydroxyapatite formation in bone. Therefore it is critical to maintain tight regulation of systemic phosphate levels. Based upon its broad biological importance, disruption of normal phosphate homeostasis has detrimental effects on skeletal integrity and overall health. Investigating heritable diseases of altered phosphate metabolism has led to key discoveries underlying the regulation and systemic actions of the phosphaturic hormone Fibroblast growth factor-23 (FGF23). Both molecular and clinical studies have revealed novel targets for the development and optimization of therapies for disorders of phosphate handling. This review will focus upon the bridge between genetic discoveries involving disorders of altered FGF23 bioactivity, as well as describe how these findings have translated into pharmacologic application.

Indexed as

AnimalsFibroblast Growth Factor-23Fibroblast Growth FactorsGenomicsHumansHypophosphatemiaInheritance PatternsPhosphatesFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPhosphatesFGF-23GeneticsHyperphosphatemiaHypophosphatemiaKlothoTumoral calcinosis

Identifiers

PMID28159712
PMCPMC5537045
OpenAlexW2583330428

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.