Evidence map›Paper›PMID 37251684›Full record

ArticleFrontiers in endocrinology2023

The crosstalk between FGF21 and GH leads to weakened GH receptor signaling and IGF1 expression and is associated with growth failure in very preterm infants.

Jayna N Mistry, Sanna Silvennoinen, Farasat Zaman, Lars Sävendahl, Katia Mariniello, Charlotte Hall, Sasha R Howard, Leo Dunkel, Ulla Sankilampi, Leonardo Guasti

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

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. 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

10 authors at 4 institutions in 3 countries.

Jayna N MistryCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Sanna SilvennoinenDepartment of Pediatrics, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
Farasat ZamanDepartment of Women's and Children's Health, Karolinska Institutet and Karolinska University, Solna, Sweden.
Lars SävendahlDepartment of Women's and Children's Health, Karolinska Institutet and Karolinska University, Solna, Sweden.
Katia MarinielloCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Charlotte HallCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Sasha R HowardCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Leo DunkelCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Ulla SankilampiDepartment of Pediatrics, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
Leonardo GuastiCentre for Endocrinology, William Harvey Research Institute, Barts and the London Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GBKarolinska Institutet · SEKuopio University Hospital · FIWilliam Harvey Research Institute · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Background: Fibroblast growth factor 21 (FGF21) is an essential metabolic regulator that adapts to changes in nutritional status. Severe childhood undernutrition induces elevated FGF21 levels, contributing to growth hormone (GH) resistance and subsequent linear growth attenuation potentially through a direct action on chondrocytes. Methods: In this study, we assessed expression of the components of both GH and FGF21 pathways in rare and unique human growth plates obtained from children. Moreover, we investigated the mechanistic interplay of FGF21 on GH receptor (GHR) signaling in a heterologous system. Results: Chronic FGF21 exposure increased GH-induced GHR turnover and SOCS2 expression, leading to the inhibition of STAT5 phosphorylation and IGF-1 expression. The clinical significance of FGF21 signaling through GH receptors was tested in nutritionally driven growth failure seen in very preterm (VPT) infants right after birth. VPT infants display an immediate linear growth failure after birth followed by growth catch-up. Consistent with the Conclusions: This study further supports a central role of FGF21 in GH resistance and linear growth failure and suggests a direct action on the growth plate.

Indexed as

Growth HormoneInsulin-Like Growth Factor IChildFibroblast Growth FactorsHumansInfantInfant, NewbornInfant, PrematureReceptors, Somatotropinfibroblast growth factor 21Fibroblast Growth FactorsGrowth HormoneIGF1 protein, humanInsulin-Like Growth Factor IReceptors, SomatotropinFGF21GH resistanceGH signalinggrowth platepreterm infants

Identifiers

PMID37251684
PMCPMC10213667
OpenAlexW4376255432

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.