Evidence map›Paper›PMID 15781582›Full record

ArticleThe Journal of experimental medicine2005

CD44 is a determinant of inflammatory bone loss.

Silvia Hayer, Günter Steiner, Birgit Görtz, Erika Reiter, Makiyeh Tohidast-Akrad, Michael Amling, Oskar Hoffmann, Kurt Redlich, Jochen Zwerina, Karl Skriner and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Emerging Landscape ofACS pharmacology & translational science · 2024
    Review
  6. The miR-29-3p family suppresses inflammatory osteolysis.Journal of cellular physiology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Modulation of unloading-induced bone loss in mice with altered ERK signaling.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  16. Article
  17. Article
  18. A pilot genome wide association and gene expression array study of suicide with and without major depression.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2013
    Article
  19. Article
  20. 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

14 authors at 8 institutions in 2 countries.

Silvia HayerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, A-1090 Vienna, Austria.
Günter Steiner
Birgit Görtz
Erika Reiter
Makiyeh Tohidast-Akrad
Michael Amling
Oskar Hoffmann
Kurt Redlich
Jochen Zwerina
Karl Skriner
Frank Hilberg
Erwin F Wagner
Josef S Smolen
Georg Schett
Medical University of Vienna · ATCeMM Research Center for Molecular Medicine · ATAustrian Academy of Sciences · ATBoehringer Ingelheim (Austria) · ATLudwig Boltzmann Institute for Digital Health and PreventionMSH Medical School Hamburg – University of Applied Sciences and Medical University · DEResearch Institute of Molecular Pathology · ATUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is a major trigger of local and systemic bone loss. Disintegration of cell-matrix interaction is a prerequisite for the invasion of inflammatory tissue into bone. CD44 is a type I transmembrane glycoprotein that connects a variety of extracellular matrix proteins to the cell surface. Tumor necrosis factor (TNF) is a major inducer of chronic inflammation and its overexpression leads to chronic inflammatory arthritis. By generating CD44(-/-) human TNF-transgenic (hTNFtg) mice, we show that destruction of joints and progressive crippling is far more severe in hTNFtg mice lacking CD44, which also develop severe generalized osteopenia. Mutant mice exhibit an increased bone resorption due to enhanced number, size, and resorptive capacity of osteoclasts, whereas bone formation and osteoblast differentiation are not affected. Responsiveness of CD44-deficient osteoclasts toward TNF is enhanced and associated with increased activation of the p38 mitogen-activated protein kinase. These data identify CD44 as a critical inhibitor of TNF-driven joint destruction and inflammatory bone loss.

Indexed as

AnimalsArthritisBone Diseases, MetabolicExtracellular MatrixGene Expression RegulationHumansHyaluronan ReceptorsInflammationMAP Kinase Signaling SystemMiceMice, KnockoutOsteoclastsOsteogenesisOsteolysisp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alphaHyaluronan Receptorsp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID15781582
PMCPMC2213110
OpenAlexW2125560549

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.