Evidence map›Paper›PMID 20634945›Full record

ArticlePloS one2010

The clock genes Period 2 and Cryptochrome 2 differentially balance bone formation.

Erik Maronde, Arndt F Schilling, Sebastian Seitz, Thorsten Schinke, Isabelle Schmutz, Gijsbertus van der Horst, Michael Amling, Urs Albrecht

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

68 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. The specificities, influencing factors, and medical implications of bone circadian rhythms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  8. Review
  9. Melatonin and bone-related diseases: an updated mechanistic overview of current evidence and future prospects.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2023
    Review
  10. Review
  11. Circadian Regulation of Macrophages and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Co-regulation of circadian clock genes and microRNAs in bone metabolism.Journal of Zhejiang University. Science. B · 2022
    Review
  17. Review
  18. Review
  19. The role of circadian rhythm in osteoporosis; a review.Frontiers in cell and developmental biology · 2022
    Review
  20. Review

8 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Erik MarondeDr. Senckenbergische Anatomie, Institute for Anatomy III, Goethe University, Frankfurt, Germany. E.Maronde@em.uni-frankfurt.de
Arndt F Schilling
Sebastian Seitz
Thorsten Schinke
Isabelle Schmutz
Gijsbertus van der Horst
Michael Amling
Urs Albrecht
Universität Hamburg · DEUniversity of Fribourg · CHGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClock genes and their protein products regulate circadian rhythms in mammals but have also been implicated in various physiological processes, including bone formation. Osteoblasts build new mineralized bone whereas osteoclasts degrade it thereby balancing bone formation. To evaluate the contribution of clock components in this process, we investigated mice mutant in clock genes for a bone volume phenotype. METHODOLOGY/PRINCIPAL

findingsWe found that Per2(Brdm1) mutant mice as well as mice lacking Cry2(-/-) displayed significantly increased bone volume at 12 weeks of age, when bone turnover is high. Per2(Brdm1) mutant mice showed alterations in parameters specific for osteoblasts whereas mice lacking Cry2(-/-) displayed changes in osteoclast specific parameters. Interestingly, inactivation of both Per2 and Cry2 genes leads to normal bone volume as observed in wild type animals. Importantly, osteoclast parameters affected due to the lack of Cry2, remained at the level seen in the Cry2(-/-) mutants despite the simultaneous inactivation of Per2. CONCLUSIONS/SIGNIFICANCE: This indicates that Cry2 and Per2 affect distinct pathways in the regulation of bone volume with Cry2 influencing mostly the osteoclastic cellular component of bone and Per2 acting on osteoblast parameters.

Indexed as

AnimalsBone DensityCryptochromesMiceMice, Mutant StrainsOsteoblastsOsteoclastsOsteogenesisPeriod Circadian ProteinsCry2 protein, mouseCryptochromesPeriod Circadian Proteins

Identifiers

PMID20634945
PMCPMC2902506
OpenAlexW2137363045

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.