Evidence map›Paper›PMID 22249518›Full record

ReviewNature reviews. Endocrinology2012

Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism.

L Darryl Quarles

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 1 pooled it
12.9field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 1 synthesis or guideline pooled it, 266 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Autosomal Recessive Hypophosphatemic Rickets Type 2 Associated with a NovelJournal of clinical research in pediatric endocrinology · 2026
    Article
  6. Review
  7. Lysophosphatidic Acid Synergizes With 1,25-Dihydroxyvitamin D to Promote Fibroblast Growth Factor-23 Synthesis via MAPK Signaling and Induction of the IL12A Gene.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

83 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

L Darryl QuarlesDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, 19 South Manassas Street, Memphis, TN 38163, USA. dquarles@uthsc.edu
University of Tennessee Health Science Center · US

Funding

Regulation and Function of FGF23R01AR045955 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI QUARLES, L DARRYL · 1999 to 2016
$4.8M
Regulation and Function of FGF23R56AR045955 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI QUARLES, L DARRYL · 2009 to 2009
$370k
NIAMS NIH HHS R01 AR045955NIAMS NIH HHS R56 AR045955
6 · The paper itself

Abstract

The discovery of fibroblast growth factor 23 (FGF-23) has expanded our understanding of phosphate and vitamin D homeostasis and provided new insights into the pathogenesis of hereditary hypophosphatemic and hyperphosphatemic disorders, as well as acquired disorders of phosphate metabolism, such as chronic kidney disease. FGF-23 is secreted by osteoblasts and osteocytes in bone and principally targets the kidney to regulate the reabsorption of phosphate, the production and catabolism of 1,25-dihydroxyvitamin D and the expression of α-Klotho, an anti-ageing hormone. Secreted FGF-23 plays a central role in complex endocrine networks involving local bone-derived factors that regulate mineralization of extracellular matrix and systemic hormones involved in mineral metabolism. Inactivating mutations of PHEX, DMP1 and ENPP1, which cause hereditary hypophosphatemic disorders and primary defects in bone mineralization, stimulate FGF23 gene transcription in osteoblasts and osteocytes, at least in part, through canonical and intracrine FGF receptor pathways. These FGF-23 regulatory pathways may enable systemic phosphate and vitamin D homeostasis to be coordinated with bone mineralization. FGF-23 also functions as a counter-regulatory hormone for 1,25-dihydroxyvitamin D in a bone-kidney endocrine loop. FGF-23, through regulation of additional genes in the kidney and extrarenal tissues, probably has broader physiological functions beyond regulation of mineral metabolism that account for the association between FGF-23 and increased mortality and morbidity in chronic kidney disease.

Indexed as

AnimalsBone and BonesFibroblast Growth Factor-23Fibroblast Growth FactorsHumansPhosphatesVitamin D1,25-dihydroxyvitamin DFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPhosphatesVitamin D

Identifiers

PMID22249518
PMCPMC4489419
OpenAlexW2166377418

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.