Evidence map›Paper›PMID 24509850›Full record

ArticleThe Journal of biological chemistry2014

FGF-23 is a negative regulator of prenatal and postnatal erythropoiesis.

Lindsay M Coe, Sangeetha Vadakke Madathil, Carla Casu, Beate Lanske, Stefano Rivella, Despina Sitara

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
4.6field-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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Erythropoietin stimulates fibroblast growth factor 23 (FGF23) in mice and men.Pflugers Archiv : European journal of physiology · 2018
    Trial
  3. Targeting FGF23 to Ameliorate Anemia in Chronic Kidney Disease.International journal of molecular sciences · 2026
    Article
  4. FGF23 - A hormone produced by bone and has many faces.Reviews in endocrine & metabolic disorders · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Anemia of Inflammation.Advances in experimental medicine and biology · 2025
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Associations between anemia and FGF23 in the CKiD study.Pediatric nephrology (Berlin, Germany) · 2024
    Article

42 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

6 authors at 3 institutions in 1 country.

Lindsay M CoeFrom the Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, New York 10010.
Sangeetha Vadakke Madathil
Carla Casu
Beate Lanske
Stefano Rivella
Despina Sitara
New York University · USCornell University · USHarvard University · US

Funding

Regulatory Role of Transferrin in Erythropoiesis and Iron MetabolismR01DK095112 · NIDDK · SAINT LOUIS UNIVERSITY · PI Robert E Fleming, Yelena Ginzburg · 2012 to 2026
$5.4M
Hepcidin therapy for iron overload and hematologic disordersR01DK090554 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI RIVELLA, STEFANO · 2010 to 2021
$5.2M
P30 Center in Craniofacial Bone BiologyP30DE020754 · NIDCR · NEW YORK UNIVERSITY · PI PARTRIDGE, NICOLA C · 2009 to 2010
$1.5M
NIDCR NIH HHS P30 DE020754NIDCR NIH HHS P30DE020754NIDDK NIH HHS R01 DK090554NIDDK NIH HHS R01 DK095112
6 · The paper itself

Abstract

Abnormal blood cell production is associated with chronic kidney disease (CKD) and cardiovascular disease (CVD). Bone-derived FGF-23 (fibroblast growth factor-23) regulates phosphate homeostasis and bone mineralization. Genetic deletion of Fgf-23 in mice (Fgf-23(-/-)) results in hypervitaminosis D, abnormal mineral metabolism, and reduced lymphatic organ size. Elevated FGF-23 levels are linked to CKD and greater risk of CVD, left ventricular hypertrophy, and mortality in dialysis patients. However, whether FGF-23 is involved in the regulation of erythropoiesis is unknown. Here we report that loss of FGF-23 results in increased hematopoietic stem cell frequency associated with increased erythropoiesis in peripheral blood and bone marrow in young adult mice. In particular, these hematopoietic changes are also detected in fetal livers, suggesting that they are not the result of altered bone marrow niche alone. Most importantly, administration of FGF-23 in wild-type mice results in a rapid decrease in erythropoiesis. Finally, we show that the effect of FGF-23 on erythropoiesis is independent of the high vitamin D levels in these mice. Our studies suggest a novel role for FGF-23 in erythrocyte production and differentiation and suggest that elevated FGF-23 levels contribute to the pathogenesis of anemia in patients with CKD and CVD.

Indexed as

AnemiaAnimalsBone MarrowCardiovascular DiseasesCell DifferentiationErythrocytesErythropoiesisFetusFibroblast Growth Factor-23Fibroblast Growth FactorsHematopoiesis, ExtramedullaryHumansLiverMiceMice, KnockoutRenal DialysisFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsVitamin DAnemiaBoneBone MarrowErythrocyteErythropoeisisFGF-23HematopoiesisKidney

Identifiers

PMID24509850
PMCPMC3975025
OpenAlexW2093187956

What OpenQuestion holds

Textmetadata
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.