Evidence map›Paper›PMID 26693137›Full record

ArticleCurrent molecular biology reports2015

Osteocytes and Skeletal Pathophysiology.

Jesus Delgado-Calle, Teresita Bellido

Open access · bronzeAbstract read
In one paragraph

Article in Current molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Immune mediated support of metastasis: Implication for bone invasion.Cancer communications (London, England) · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. The osteocyte as a signaling cell.Physiological reviews · 2022
    Review
  14. Review
  15. Review
  16. The multifunctional role of Notch signaling in multiple myeloma.Journal of cancer metastasis and treatment · 2021
    Article
  17. Erythropoietin signaling in osteoblasts is required for normal bone formation and for bone loss during erythropoietin-stimulated erythropoiesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  18. Review
  19. Review
  20. Sclerostin Antibody Treatment Increases Bone Mass and Normalizes Circulating Phosphate Levels in Growing Hyp Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    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

2 authors at 2 institutions in 1 country.

Jesus Delgado-CalleDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana ; Roudebush Veterans Administration Medical Center, Indianapolis, Indiana.
Teresita BellidoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana ; Department of Medicine, Division of Endocrinology, Indiana University School of Medicine, Indianapolis, Indiana ; Roudebush Veterans Administration Medical Center, Indianapolis, Indiana.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Glucocorticoid-induced Atrophy in Bone and MuscleR01AR059357 · NIAMS · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M. · 2011 to 2022
$3.4M
Osteocyte control of bone formation via SostR01DK076007 · NIDDK · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M. · 2007 to 2010
$1.4M
SkyScan 1172 High-resolution desk-top micro-CT systemS10RR023710 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI WILLIAMS, JAMES C · 2007 to 2007
$297k
PTH receptor Signaling and Diabetes-induced Bone DiseaseI01BX002104 · VA · RLR VA MEDICAL CENTER · PI BELLIDO, TERESITA M. · 2014 to 2023
–
BLRD VA I01 BX002104BLRD VA IK6 BX004596NCRR NIH HHS S10 RR023710NIAMS NIH HHS R01 AR059357NIDDK NIH HHS R01 DK076007
6 · The paper itself

Abstract

For many years, osteocytes have been the forgotten bone cells and considered as inactive spectators buried in the bone matrix. We now know that osteocytes detect and respond to mechanical and hormonal stimuli to coordinate bone resorption and bone formation. Osteocytes are currently considered a major source of molecules that regulate the activity of osteoclasts and osteoblasts, such as RANKL and sclerostin; and genetic and pharmacological manipulations of either molecule markedly affect bone homeostasis. Besides playing a role in physiological bone homeostasis, accumulating evidence supports the notion that dysregulation of osteocyte function and alteration of osteocyte life-span underlies the pathophysiology of skeletal disorders characterized by loss bone mass and increased bone fragility, as well as the damaging effects of cancer in bone. In this review, we highlight some of these investigations and discuss novel observations that demonstrate that osteocytes, far from being passive cells entombed in the bone, are critical for bone function and maintenance.

Indexed as

bone remodelingosteoblastosteoclastosteocyteSOSTWnt signaling

Identifiers

PMID26693137
PMCPMC4673661
OpenAlexW1834427752

What OpenQuestion holds

Textmetadata
LicenceTDM
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.