Evidence map›Paper›PMID 30120363›Full record

ArticleScientific reports2018

Cardiovascular Interactions between Fibroblast Growth Factor-23 and Angiotensin II.

Min Pi, Ruisong Ye, Xiaobin Han, Benjamin Armstrong, Xue Liu, Yuanjian Chen, Yao Sun, L Darryl Quarles

Open access · goldAbstract read
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 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Min PiDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Ruisong YeDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Xiaobin HanDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Benjamin ArmstrongDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Xue LiuDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Yuanjian ChenDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Yao SunDivision of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
L Darryl QuarlesDivision of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA. dquarles@uthsc.edu.
University 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
Regulatory Mechanisms of Oxidative Stress in Cardiac Angiogenesis PostinfarctionR01HL096503 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, YAO · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL096503NIAMS NIH HHS R01 AR045955U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) 1RO1-HL096503U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) 1RO1-AR045955
6 · The paper itself

Abstract

Both the activation of the renin angiotensin aldosterone system (RAAS) and elevations of circulating Fibroblast Growth Factor-23 (FGF-23) have been implicated in the pathogenesis of left ventricular hypertrophy (LVH) in chronic kidney disease. To investigate potential cross-talk between RAAS and FGF-23, we administered angiotensin II (Ang II) to wild-type rodents and the Hyp mouse model of excess FGF-23. Ang II administration for four weeks to wild-type rodents resulted in significant increases in systolic blood pressure and LVH. Unexpectedly, FGF-23 circulating levels were increased by 1.5-1.7 fold in Ang II treated animals. In addition, Ang II treatment increased expression of FGF-23 message levels in bone, the predominant tissue for FGF-23 production, and induced expression of FGF-23 and its co-receptor α-Klotho in the heart, which normally does not express FGF-23 or α-Klotho in physiologically relevant levels. Hyp mice with elevated FGF-23 exhibited increased blood pressure and LVH at baseline. Ang II administration to Hyp mice resulted further increments in blood pressure and left ventricular hypertrophy, consistent with additive cardiovascular effects. These findings suggest that FGF-23 may participate in unexpected systemic and paracrine networks regulating hemodynamic and myocardial responses.

Indexed as

Angiotensin IIAnimalsBlood PressureCardiovascular DiseasesDisease Models, AnimalEchocardiographyFibroblast Growth Factor-23Fibroblast Growth FactorsGene ExpressionMaleMiceMice, KnockoutMyocardiumRatsRodentiaSignal TransductionAngiotensin IIFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth Factors

Identifiers

PMID30120363
PMCPMC6098163
OpenAlexW2886002784

What OpenQuestion holds

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LicenceCC BY
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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.