Evidence map›Paper›PMID 29096595›Full record

ReviewToxicologic pathology2017

Pleiotropic Actions of FGF23.

Reinhold G Erben

Open access · hybridAbstract readReview
In one paragraph

Review in Toxicologic pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Regulation of 1 and 24 hydroxylation of vitamin D metabolites in the proximal tubule.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Genetic renal disease classification by hormonal axes.Pediatric nephrology (Berlin, Germany) · 2020
    Review
  13. Review
  14. Sclerostin Antibody Treatment Increases Bone Mass and Normalizes Circulating Phosphate Levels in Growing Hyp Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  15. A Mutation inFrontiers in cell and developmental biology · 2020
    Article
  16. FGF23 and bone microarchitecture.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2019
    Article
  17. The Role of Fibroblast Growth Factor 23 in Inflammation and Anemia.International journal of molecular sciences · 2019
    Review
  18. Article
  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

1 author at 1 institution in 1 country.

Reinhold G Erben1 Department of Biomedical Sciences, Institute of Physiology, Pathophysiology and Biophysics, University of Veterinary Medicine, Vienna, Austria.
University of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF P 24186
6 · The paper itself

Abstract

Fibroblast growth factor-23 (FGF23) is a bone-derived hormone, mainly produced by osteoblasts and osteocytes in response to increased extracellular phosphate and circulating vitamin D hormone. Endocrine FGF23 signaling requires co-expression of the ubiquitously expressed FGF receptor 1 (FGFR1) and the co-receptor α-Klotho (Klotho). In proximal renal tubules, FGF23 suppresses the membrane expression of the sodium-phosphate cotransporters Npt2a and Npt2c which mediate urinary reabsorption of filtered phosphate. In addition, FGF23 suppresses proximal tubular expression of 1α-hydroxylase, the key enzyme responsible for vitamin D hormone production. In distal renal tubules, FGF23 signaling activates with-no-lysine kinase 4, leading to increased renal tubular reabsorption of calcium and sodium. Therefore, FGF23 is not only a phosphaturic but also a calcium- and sodium-conserving hormone, a finding that may have important implications for the pathophysiology of chronic kidney disease. Besides these endocrine, Klotho-dependent functions of FGF23, FGF23 is also an auto-/paracrine suppressor of tissue-nonspecific alkaline phosphatase transcription via Klotho-independent FGFR3 signaling, leading to local inhibition of mineralization through accumulation of pyrophosphate. In addition, FGF23 may target the heart via an FGFR4-mediated Klotho-independent signaling cascade. Taken together, there is emerging evidence that FGF23 is a pleiotropic hormone, linking bone with several other organ systems.

Indexed as

Autocrine CommunicationBone and BonesCalcification, PhysiologicCardiovascular SystemFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHumansImmunomodulationKidney Tubules, ProximalKlotho ProteinsParacrine CommunicationPhosphatesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3Receptor, Fibroblast Growth Factor, Type 4FGF23 protein, humanFGFR1 protein, humanFGFR3 protein, humanFGFR4 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphatesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3Receptor, Fibroblast Growth Factor, Type 4SLC34A1 protein, humanSLC34A3 protein, humanSodium-Phosphate Cotransporter Proteins, Type IIaSodium-Phosphate Cotransporter Proteins, Type IIcbonebone mineralizationcardiovascular systemendocrine systemmineral metabolismrenaltransgenic animals

Identifiers

PMID29096595
PMCPMC6154255
OpenAlexW2766156530

What OpenQuestion holds

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LicenceCC BY
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.