Evidence map›Paper›PMID 22298654›Full record

ReviewPhysiological reviews2012

Regulation and function of the FGF23/klotho endocrine pathways.

Aline Martin, Valentin David, L Darryl Quarles

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 293 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
293citing papers in PubMed, 3 pooled it
23.6field-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

293 citing papers in PubMed, 3 syntheses or guidelines pooled it, 578 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Erythropoietin stimulates fibroblast growth factor 23 (FGF23) in mice and men.Pflugers Archiv : European journal of physiology · 2018
    Trial
  6. Trial
  7. Review
  8. Article
  9. Article
  10. Bone as an endocrine regulator of lipid and energy metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  11. Review
  12. Article
  13. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  14. Article
  15. Fibroblast Growth Factor 23, Urinary Phosphate, and Risk of Progression of CKD.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

233 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

3 authors at 1 institution in 1 country.

Aline MartinUniversity of Tennessee Health Science Center, Memphis, Tennessee, USA.
Valentin David
L Darryl Quarles
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
NIAMS NIH HHS R01 AR045955
6 · The paper itself

Abstract

Calcium (Ca(2+)) and phosphate (PO(4)(3-)) homeostasis are coordinated by systemic and local factors that regulate intestinal absorption, influx and efflux from bone, and kidney excretion and reabsorption of these ions through a complex hormonal network. Traditionally, the parathyroid hormone (PTH)/vitamin D axis provided the conceptual framework to understand mineral metabolism. PTH secreted by the parathyroid gland in response to hypocalcemia functions to maintain serum Ca(2+) levels by increasing Ca(2+) reabsorption and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] production by the kidney, enhancing Ca(2+) and PO(4)(3-) intestinal absorption and increasing Ca(2+) and PO(4)(3-) efflux from bone, while maintaining neutral phosphate balance through phosphaturic effects. FGF23 is a recently discovered hormone, predominately produced by osteoblasts/osteocytes, whose major functions are to inhibit renal tubular phosphate reabsorption and suppress circulating 1,25(OH)(2)D levels by decreasing Cyp27b1-mediated formation and stimulating Cyp24-mediated catabolism of 1,25(OH)(2)D. FGF23 participates in a new bone/kidney axis that protects the organism from excess vitamin D and coordinates renal PO(4)(3-) handling with bone mineralization/turnover. Abnormalities of FGF23 production underlie many inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts.

Indexed as

AnimalsCalciumEndocrine SystemFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHomeostasisHumansKlotho ProteinsPhosphatesSignal TransductionCalciumFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphates

Identifiers

PMID22298654
PMCPMC3306265
OpenAlexW2129321769

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.