Evidence map›Paper›PMID 26527066›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Enhanced FGF23 production in mice expressing PI3K-insensitive GSK3 is normalized by β-blocker treatment.

Abul Fajol, Hong Chen, Anja T Umbach, L Darryl Quarles, Florian Lang, Michael Föller

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  3. Review
  4. The regulation of FGF23 under physiological and pathophysiological conditions.Pflugers Archiv : European journal of physiology · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Insulin suppresses the production of fibroblast growth factor 23 (FGF23).Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Review
  12. Paracrine Effects of FGF23 on the Heart.Frontiers in endocrinology · 2018
    Review
  13. Article
  14. Review
  15. Extrarenal effects of FGF23.Pediatric nephrology (Berlin, Germany) · 2017
    Review
  16. Review
  17. Article
  18. FGF23 from bench to bedside.American journal of physiology. Renal physiology · 2016
    Review
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 2 countries.

Abul Fajol*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany.
Hong Chen*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany.
Anja T Umbach*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany.
L Darryl Quarles*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany.
Florian Lang*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany.
Michael Föller*Department of Physiology, University of Tübingen, Tübingen, Germany; Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA; and Institute of Agricultural and Nutritional Sciences, Martin Luther University of Halle-Wittenberg, Halle, Germany michael.foeller@landw.uni-halle.de.
University of Tübingen · DEMartin Luther University Halle-Wittenberg · DEUniversity 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

Glycogen synthase kinase (GSK)-3 is a ubiquitously expressed kinase inhibited by insulin-dependent Akt/PKB/SGK. Mice expressing Akt/PKB/SGK-resistant GSK3α/GSK3β (gsk3(KI)) exhibit enhanced sympathetic nervous activity and phosphaturia with decreased bone density. Hormones participating in phosphate homeostasis include fibroblast growth factor (FGF)-23, a bone-derived hormone that inhibits 1,25-dihydroxyvitamin D3 (1,25(OH)2D3; calcitriol) formation and phosphate reabsorption in the kidney and counteracts vascular calcification and aging. FGF23 secretion is stimulated by the sympathetic nervous system. We studied the role of GSK3-controlled sympathetic activity in FGF23 production and phosphate metabolism. Serum FGF23, 1,25(OH)2D3, and urinary vanillylmandelic acid (VMA) were measured by ELISA, and serum and urinary phosphate and calcium were measured by photometry in gsk3(KI) and gsk3(WT) mice, before and after 1 wk of oral treatment with the β-blocker propranolol. Urinary VMA excretion, serum FGF23, and renal phosphate and calcium excretion were significantly higher, and serum 1,25(OH)2D3 and phosphate concentrations were lower in gsk3(KI) mice than in gsk3(WT) mice. Propranolol treatment decreased serum FGF23 and loss of renal calcium and phosphate and increased serum phosphate concentration in gsk3(KI) mice. We conclude that Akt/PKB/SGK-sensitive GSK3 inhibition participates in the regulation of FGF23 release, 1,25(OH)2D3 formation, and thus mineral metabolism, by controlling the activity of the sympathetic nervous system.

Indexed as

Adrenergic beta-AntagonistsAnimalsCalcitriolCalciumFibroblast Growth Factor-23Fibroblast Growth FactorsGlycogen Synthase Kinase 3KidneyMiceMice, Mutant StrainsPhosphatesPhosphatidylinositol 3-KinasesPropranololVanilmandelic AcidAdrenergic beta-AntagonistsCalcitriolCalciumFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsGlycogen Synthase Kinase 3PhosphatesPhosphatidylinositol 3-KinasesPropranololVanilmandelic Acidcalcitriolpropranololprotein kinase Bsympathetic activity

Identifiers

PMID26527066
PMCPMC6994240
OpenAlexW2186406054

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.