Evidence map›Paper›PMID 28900153›Full record

ArticleScientific reports2017

Genetic Ablation of Fgf23 or Klotho Does not Modulate Experimental Heart Hypertrophy Induced by Pressure Overload.

Svetlana Slavic, Kristopher Ford, Magalie Modert, Amarela Becirovic, Stephan Handschuh, Andreas Baierl, Nejla Katica, Ute Zeitz, Reinhold G Erben, Olena Andrukhova

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.0field-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

43 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
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  6. Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025
    Review
  7. Article
  8. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Review
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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

10 authors at 2 institutions in 1 country.

Svetlana SlavicDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Kristopher FordDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Magalie ModertDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Amarela BecirovicDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Stephan HandschuhVetCore, University of Veterinary Medicine Vienna, Vienna, Austria.
Andreas BaierlDepartment of Statistics and Operations Research, University of Vienna, Vienna, Austria.
Nejla KaticaDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Ute ZeitzDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Reinhold G ErbenDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Olena AndrukhovaDepartment of Biomedical Sciences, University of Veterinary Medicine Vienna, Vienna, Austria. Olena.Andrukhova@vetmeduni.ac.at.
University of Veterinary Medicine Vienna · ATUniversity of Vienna · AT

Funding

Austrian Science Fund FWF P 26534
6 · The paper itself

Abstract

Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage. Aldosterone receptor blocker spironolactone normalizes serum intact Fgf23 levels after TAC by reducing bony Fgf23 transcription. Notably, genetic Fgf23 or Klotho deficiency does not influence TAC-induced hypertrophic remodelling, LV functional impairment, or LV fibrosis. Despite the profound, aldosterone-mediated increase in circulating intact Fgf23 after TAC, our data do not support an essential role of Fgf23 or Klotho in the pathophysiology of pressure overload-induced cardiac hypertrophy.

Indexed as

Gene Knockout TechniquesAldosteroneAnimalsBiomarkersBlood PressureCardiomegalyDisease Models, AnimalDisease SusceptibilityFibroblast Growth Factor-23Fibroblast Growth FactorsFibrosisGene Expression RegulationGlucuronidaseKlotho ProteinsMiceMice, KnockoutAldosteroneBiomarkersFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsSpironolactone

Identifiers

PMID28900153
PMCPMC5595838
OpenAlexW2753892294

What OpenQuestion holds

Textmetadata
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.