Evidence map›Paper›PMID 22442678›Full record

Trial reportPloS one2012

Ablation of the pro-apoptotic protein Bax protects mice from glucocorticoid-induced bone growth impairment.

Farasat Zaman, Dionisios Chrysis, Kirsten Huntjens, Bengt Fadeel, Lars Sävendahl

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Humanin is a novel regulator of Hedgehog signaling and prevents glucocorticoid-induced bone growth impairment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Article
  9. Article
  10. Bone: Safer glucocorticoid therapy--Bax to the future?Nature reviews. Rheumatology · 2012
    Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Farasat ZamanPediatric Endocrinology Unit, Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden. Farasat.Zaman@ki.se
Dionisios Chrysis
Kirsten Huntjens
Bengt Fadeel
Lars Sävendahl
Karolinska Institutet · SESachs' Children and Youth Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dexamethasone (Dexa) is a widely used glucocorticoid to treat inflammatory diseases; however, a multitude of undesired effects have been reported to arise from this treatment including osteoporosis, obesity, and in children decreased longitudinal bone growth. We and others have previously shown that glucocorticoids induce apoptosis in growth plate chondrocytes. Here, we hypothesized that Bax, a pro-apoptotic member of the Bcl-2 family, plays a key role in Dexa-induced chondrocyte apoptosis and bone growth impairment. Indeed, experiments in the human HCS-2/8 chondrocytic cell line demonstrated that silencing of Bax expression using small-interfering (si) RNA efficiently blocked Dexa-induced apoptosis. Furthermore, ablation of Bax in female mice protected against Dexa-induced bone growth impairment. Finally, Bax activation by Dexa was confirmed in human growth plate cartilage specimens cultured ex vivo. Our findings could therefore open the door for new therapeutic approaches to prevent glucocorticoid-induced bone growth impairment through specific targeting of Bax.

Indexed as

DexamethasoneGlucocorticoidsAdolescentAnimalsApoptosisbcl-2-Associated X ProteinCell LineChondrocytesFemaleGrowth PlateHumansMaleMiceMice, Mutant StrainsObesityOsteoporosisBAX protein, humanBax protein, mousebcl-2-Associated X ProteinDexamethasoneGlucocorticoids

Identifiers

PMID22442678
PMCPMC3307731
OpenAlexW2058598121

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.