Evidence map›Paper›PMID 36307458›Full record

ArticleScientific reports2022

TNF overexpression and dexamethasone treatment impair chondrogenesis and bone growth in an additive manner.

Yunhan Zhao, Bettina Celvin, Maria C Denis, Niki Karagianni, Cecilia Aulin, Farasat Zaman, Lars Sävendahl

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. 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
0.8field-weighted citation impact, top 31% 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, 9 citations in OpenAlex.

  1. Pooled it
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  9. MultiplebioRxiv : the preprint server for biology · 2023
    Article
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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

7 authors at 3 institutions in 2 countries.

Yunhan ZhaoDepartment of Women's and Children´s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, J9:30, Visionsgatan 4, 171 64, Solna, Sweden. yunhan.zhao.1@ki.se.
Bettina CelvinDepartment of Women's and Children´s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, J9:30, Visionsgatan 4, 171 64, Solna, Sweden.
Maria C DenisBiomedcode Hellas S.A., 34 Al. Fleming Str, 16672, Vari, Greece.
Niki KaragianniBiomedcode Hellas S.A., 34 Al. Fleming Str, 16672, Vari, Greece.
Cecilia AulinDepartment of Medicine Solna, Karolinska Institutet and Division of Rheumatology, Karolinska University Hospital, Center for Molecular Medicine, Visionsgatan 18, 171 76, Solna, Sweden.
Farasat Zaman *Department of Women's and Children´s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, J9:30, Visionsgatan 4, 171 64, Solna, Sweden.
Lars Sävendahl *Department of Women's and Children´s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, J9:30, Visionsgatan 4, 171 64, Solna, Sweden.
Karolinska Institutet · SEAlexander Fleming Biomedical Sciences Research Center · GRKarolinska University Hospital · SE

Funding

Vetenskapsrådet 2020-02025
6 · The paper itself

Abstract

Children with chronic inflammation are often treated with glucocorticoids (GCs) and many of them experience growth retardation. It is poorly understood how GCs interact with inflammatory cytokines causing growth failure as earlier experimental studies have been performed in healthy animals. To address this gap of knowledge, we used a transgenic mouse model where human TNF is overexpressed (huTNFTg) leading to chronic polyarthritis starting from the first week of age. Our results showed that femur bone length and growth plate height were significantly decreased in huTNFTg mice compared to wild type animals. In the growth plates of huTNFTg mice, increased apoptosis, suppressed Indian hedgehog, decreased hypertrophy, and disorganized chondrocyte columns were observed. Interestingly, the GC dexamethasone further impaired bone growth, accelerated chondrocyte apoptosis and reduced the number of chondrocyte columns in huTNFTg mice. We conclude that TNF and dexamethasone separately suppress chondrogenesis and bone growth when studied in an animal model of chronic inflammation. Our data give a possible mechanistic explanation to the commonly observed growth retardation in children with chronic inflammatory diseases treated with GCs.

Indexed as

ChondrogenesisHedgehog ProteinsAnimalsBone DevelopmentChildChondrocytesDexamethasoneGlucocorticoidsGrowth DisordersGrowth PlateHumansInflammationMiceMice, TransgenicDexamethasoneGlucocorticoidsHedgehog Proteins

Identifiers

PMID36307458
PMCPMC9616891
OpenAlexW4307475981

What OpenQuestion holds

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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.