Evidence map›Paper›PMID 29588427›Full record

ReviewJournal of molecular endocrinology2018

Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture.

Yasmine Hachemi, Anna E Rapp, Ann-Kristin Picke, Gilbert Weidinger, Anita Ignatius, Jan Tuckermann

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.5field-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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Inhibition of Fin Regeneration in Fathead Minnow (Environmental science & technology · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Advances in Diagnosis and Management of Childhood OsteoporosisJournal of clinical research in pediatric endocrinology · 2022
    Review
  18. Review
  19. Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?International journal of molecular sciences · 2022
    Review
  20. Antioxidants (Basel, Switzerland) · 2022
    Article
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

6 authors at 2 institutions in 1 country.

Yasmine HachemiInstitute of Comparative Molecular EndocrinologyUlm University, Ulm, Germany.
Anna E RappInstitute of Orthopaedic Research and BiomechanicsUlm University Medical Centre, Ulm, Germany.
Ann-Kristin PickeInstitute of Comparative Molecular EndocrinologyUlm University, Ulm, Germany.
Gilbert WeidingerInstitute of Biochemistry and Molecular BiologyUlm University, Ulm, Germany.
Anita IgnatiusInstitute of Orthopaedic Research and BiomechanicsUlm University Medical Centre, Ulm, Germany.
Jan TuckermannInstitute of Comparative Molecular EndocrinologyUlm University, Ulm, Germany jan.tuckermann@uni-ulm.de.
Universität Ulm · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid hormones (GCs) have profound effects on bone metabolism. Via their nuclear hormone receptor - the GR - they act locally within bone cells and modulate their proliferation, differentiation, and cell death. Consequently, high glucocorticoid levels - as present during steroid therapy or stress - impair bone growth and integrity, leading to retarded growth and glucocorticoid-induced osteoporosis, respectively. Because of their profound impact on the immune system and bone cell differentiation, GCs also affect bone regeneration and fracture healing. The use of conditional-mutant mouse strains in recent research provided insights into the cell-type-specific actions of the GR. However, despite recent advances in system biology approaches addressing GR genomics in general, little is still known about the molecular mechanisms of GCs and GR in bone cells. Here, we review the most recent findings on the molecular mechanisms of the GR in general and the known cell-type-specific actions of the GR in mesenchymal cells and their derivatives as well as in osteoclasts during bone homeostasis, GC excess, bone regeneration and fracture healing.

Indexed as

AnimalsBone RegenerationFracture HealingGlucocorticoidsHumansOsteoblastsOsteoclastsReceptors, GlucocorticoidSkeletonGlucocorticoidsReceptors, Glucocorticoidbone regenerationfracture healingglucocorticoid receptorosteoblastosteoclast

Identifiers

PMID29588427
PMCPMC5976078
OpenAlexW2794774376

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.