Evidence map›Paper›PMID 27219043›Full record

ReviewCurrent opinion in nephrology and hypertension2016

The role of fibroblast growth factor 23 and Klotho in uremic cardiomyopathy.

Alexander Grabner, Christian Faul

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.8field-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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  15. Review
  16. Uraemic Cardiomyopathy: A Review of Current Literature.Clinical Medicine Insights. Cardiology · 2021
    Review
  17. Article
  18. Review
  19. A Land of Controversy: Fibroblast Growth Factor-23 and Uremic Cardiac Hypertrophy.Journal of the American Society of Nephrology : JASN · 2020
    Review
  20. 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

2 authors at 2 institutions in 1 country.

Alexander GrabneraKatz Family Drug Discovery Center and Division of Nephrology and Hypertension, Department of Medicine bDepartment of Cell Biology and Anatomy, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA.
Christian Faul
Children’s Institute · USStar Center · US

Funding

ACTIVATION OF CARDIAC FGFR4 CAUSES LEFT VENTRICULAR HYPERTROPHYR01HL128714 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FAUL, CHRISTIAN · 2015 to 2019
$1.9M
NHLBI NIH HHS R01 HL128714
6 · The paper itself

Abstract

purpose of reviewIn chronic kidney disease (CKD), multiple factors contribute to the development of cardiac hypertrophy by directly targeting the heart or indirectly by inducing systemic changes such as hypertension, anemia, and inflammation. Furthermore, disturbances in phosphate metabolism have been identified as nonclassical risk factors for cardiovascular mortality in these patients. With declining kidney function, the physiologic regulators of phosphate homeostasis undergo changes in their activity as well as their circulating levels, thus potentially contributing to cardiac hypertrophy once they are out of balance. Recently, two of these phosphate regulators, fibroblast growth factor 23 (FGF23) and Klotho, have been shown to affect cardiac remodeling, thereby unveiling a novel pathomechanism of cardiac hypertrophy in CKD. Here we discuss the potential direct versus indirect effects of FGF23 and the soluble form of Klotho on the heart, and their crosstalk in the regulation of cardiac hypertrophy. RECENT

findingsIn models of CKD, FGF23 can directly target cardiac myocytes via FGF receptor 4 and induce cardiac hypertrophy in a blood pressure-independent manner. Soluble Klotho may directly target the heart via an unknown receptor thereby protecting the myocardium from pathologic stress stimuli that are associated with CKD, such as uremic toxins or FGF23. SUMMARY: Elevated serum levels of FGF23 and reduced serum levels of soluble Klotho contribute to uremic cardiomyopathy in a synergistic manner.

Indexed as

CardiomegalyCardiomyopathiesFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHumansKlotho ProteinsMyocardiumPhosphatesRenal Insufficiency, ChronicUremiaFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphates

Identifiers

PMID27219043
PMCPMC4891254
OpenAlexW2396532096

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.