Evidence map›Paper›PMID 27191351›Full record

ReviewCurrent opinion in nephrology and hypertension2016

Inflammation regulates fibroblast growth factor 23 production.

Connor Francis, Valentin David

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 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The effects of tenapanor on serum fibroblast growth factor 23 in patients receiving hemodialysis with hyperphosphatemia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
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  16. Effect of Diosmin on Selected Parameters of Oxygen Homeostasis.International journal of molecular sciences · 2023
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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

2 authors at 1 institution in 1 country.

Connor FrancisaDivision of Nephrology and Hypertension, Department of Medicine bCenter for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Valentin David
Northwestern University · US

Funding

Regulation of FGF23 in Chronic Kidney Disease (CKD) by iron and inflammationR01DK102815 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DAVID, NICOLAE VALENTIN · 2015 to 2024
$4.9M
NIDDK NIH HHS R01 DK102815
6 · The paper itself

Abstract

purpose of reviewFibroblast growth factor 23 (FGF23) is a hormone secreted by osteocytes and osteoblasts that regulates phosphorus and vitamin D homeostasis. FGF23 levels increase progressively in chronic kidney disease (CKD), and FGF23 excess might be a causal factor of left ventricular hypertrophy, CKD progression and death. Therefore, understanding the molecular mechanisms that control FGF23 production is critical to design therapies to lower FGF23 levels. The present review focuses on the role of inflammatory stimuli on FGF23 regulation and summarizes recent studies that support a novel framework linking inflammation to FGF23 regulation. RECENT

findingsInflammation and iron deficiency, which are common occurrences in CKD, have emerged as novel FGF23 regulators. Recent findings show that inflammation increases FGF23 production in bone through direct and iron-related indirect mechanisms. In these settings, hypoxia-inducible factor (HIF)-1α orchestrates FGF23 transcription in response to inflammation and is primarily responsible for coordinating FGF23 production and cleavage. SUMMARY: We demonstrate that inflammation increases FGF23 production and may contribute to elevated FGF23 levels in CKD. Osseous HIF-1α may represent a therapeutic target to lower FGF23 levels in CKD patients and minimize the negative consequences associated with FGF23 excess.

Indexed as

Bone and BonesDiseaseDisease ProgressionFibroblast Growth Factor-23Fibroblast Growth FactorsHomeostasisHumansHypertrophy, Left VentricularHypoxia-Inducible Factor 1, alpha SubunitInflammationIronOsteoblastsOsteocytesPhosphorusRenal Insufficiency, ChronicVitamin DFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIronPhosphorusVitamin D

Identifiers

PMID27191351
PMCPMC5016608
OpenAlexW2407151017

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.