Evidence map›Paper›PMID 29849175›Full record

ArticleScientific reports2018

Klotho is upregulated in human cardiomyopathy independently of circulating Klotho levels.

G Poelzl, S K Ghadge, M Messner, B Haubner, Ph Wuertinger, A Griesmacher, J Doerler, C Ensinger, H Ulmer, M M Zaruba

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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 1 institution in 1 country.

G PoelzlDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
S K GhadgeDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
M MessnerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
B HaubnerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
Ph WuertingerCentral Institute for Medical and Chemical Laboratory Diagnosis, Medical University of Innsbruck, Innsbruck, Austria.
A GriesmacherCentral Institute for Medical and Chemical Laboratory Diagnosis, Medical University of Innsbruck, Innsbruck, Austria.
J DoerlerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.
C EnsingerDepartment of Pathology, Medical University of Innsbruck, Innsbruck, Austria.
H UlmerDepartment of Medical Statistics, Informatics and Health Economics, Medical University of Innsbruck, Innsbruck, Austria.
M M ZarubaDepartment of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria. Marc-Michael.Zaruba@i-med.ac.at.ORCID 0000-0003-1074-5463
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Klotho is an antiaging protein which exerts known cardioprotection. In kidney, trans-membrane Klotho acts as essential co-receptor of fibroblast growth factor 23 (FGF23). In the heart, soluble Klotho (sKlotho) protects from systolic dysfunction independently of FGF23. Here, we analyzed the association of FGF23 and sKlotho upon progression of chronic heart failure (CHF) and analyzed Klotho expression in human hearts. Serum levels of sKlotho and FGF23 were measured in 287 patients with cardiomyopathy (CMP). Tissue samples from CMP (n = 10) and healthy control hearts (n = 10) were analyzed for Klotho mRNA and protein expression. Individuals in the first FGF23 tertile were 4.1 times more likely of freedom from death, heart transplantation or assist device implantation compared to third tertile. No relationship was found between sKlotho and the combined endpoint. Instead, Klotho mRNA encoding the full-length form was upregulated in human CMP hearts. Immunoblotting confirmed upregulation of sKlotho associated with increased expression of proteases involved in cleavage of Klotho suggesting rather local effects of Klotho in the heart. Therefore, we conclude that in contrast to FGF23, serum sKlotho is not associated with disease severity or progression in CHF. Instead, Klotho is expressed and upregulated in diseased hearts, suggesting local paracrine effects.

Indexed as

Up-RegulationAdultCardiomyopathiesCohort StudiesDisease ProgressionFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHeart FailureHumansKlotho ProteinsMaleMiddle AgedRNA, MessengerFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsRNA, Messenger

Identifiers

PMID29849175
PMCPMC5976633
OpenAlexW2806609366

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.