Evidence map›Paper›PMID 25679016›Full record

ArticleGenes & diseases2014

Fibroblast growth factor (FGF) signaling in development and skeletal diseases.

Chad M Teven, Evan M Farina, Jane Rivas, Russell R Reid

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

Article in Genes & diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 3 pooled it
5.8field-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

122 citing papers in PubMed, 3 syntheses or guidelines pooled it, 235 citations in OpenAlex.

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62 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Chad M TevenThe Laboratory of Craniofacial Biology, Section of Plastic & Reconstructive Surgery, Department of Surgery, The University of Chicago Medical Center, 5841 South Maryland Avenue, MC 6035, Chicago, IL 60637, USA.
Evan M FarinaThe University of Chicago Pritzker School of Medicine, Chicago, IL 60637, USA.
Jane RivasThe University of Chicago Pritzker School of Medicine, Chicago, IL 60637, USA.
Russell R ReidThe Laboratory of Craniofacial Biology, Section of Plastic & Reconstructive Surgery, Department of Surgery, The University of Chicago Medical Center, 5841 South Maryland Avenue, MC 6035, Chicago, IL 60637, USA.
University of Chicago · USUniversity of Chicago Medical Center · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Short Term Training: Health Professional StudentsT35DK062719 · NIDDK · UNIVERSITY OF CHICAGO · PI CHANG, EUGENE B · 2003 to 2017
$2.9M
Differential Effects of BMPs on the Healing of Craniofacial DefectsK08DE020140 · NIDCR · UNIVERSITY OF CHICAGO · PI REID, RUSSELL R. · 2009 to 2013
$624k
NCATS NIH HHS UL1 TR000430NIDCR NIH HHS K08 DE020140NIDDK NIH HHS T35 DK062719
6 · The paper itself

Abstract

Fibroblast growth factors (FGF) and their receptors serve many functions in both the developing and adult organism. Humans contain 18 FGF ligands and four FGF receptors (FGFR). FGF ligands are polypeptide growth factors that regulate several developmental processes including cellular proliferation, differentiation, and migration, morphogenesis, and patterning. FGF-FGFR signaling is also critical to the developing axial and craniofacial skeleton. In particular, the signaling cascade has been implicated in intramembranous ossification of cranial bones as well as cranial suture homeostasis. In the adult, FGFs and FGFRs are crucial for tissue repair. FGF signaling generally follows one of three transduction pathways: RAS/MAP kinase, PI3/AKT, or PLCγ. Each pathway likely regulates specific cellular behaviors. Inappropriate expression of FGF and improper activation of FGFRs are associated with various pathologic conditions, unregulated cell growth, and tumorigenesis. Additionally, aberrant signaling has been implicated in many skeletal abnormalities including achondroplasia and craniosynostosis. The biology and mechanisms of the FGF family have been the subject of significant research over the past 30 years. Recently, work has focused on the therapeutic targeting and potential of FGF ligands and their associated receptors. The majority of FGF-related therapy is aimed at age-related disorders. Increased understanding of FGF signaling and biology may reveal additional therapeutic roles, both in utero and postnatally. This review discusses the role of FGF signaling in general physiologic and pathologic embryogenesis and further explores it within the context of skeletal development.

Indexed as

CraniosynostosisFGF signalingFibroblast growth factorFibroblast growth factor receptorGeneticsPathogenesisSignal transductionSkeletal development

Identifiers

PMID25679016
PMCPMC4323088
OpenAlexW2026663929

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.