Evidence map›Paper›PMID 27742498›Full record

ReviewBone2017

Role and mechanism of action of sclerostin in bone.

Jesus Delgado-Calle, Amy Y Sato, Teresita Bellido

Abstract readReview
In one paragraph

Review in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 2 pooled it
12.0field-weighted citation impact, top 1% 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

234 citing papers in PubMed, 2 syntheses or guidelines pooled it, 425 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Effects of progesterone therapy on serum sclerostin levels in healthy menopausal women: a 3-month randomized, placebo-controlled clinical trial.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2020
    Trial
  5. Article
  6. Bone reports · 2026
    Article
  7. Article
  8. Review
  9. Clinical insights into the association between chronic liver disease and osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Review
  10. Review
  11. Review
  12. Review
  13. Impact of oral glucocorticoids on the effectiveness of romosozumab: the multicenter OASIS cohort study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Observational
  14. Review
  15. Review
  16. Upregulation of Parathyroid Hormone Receptor 1 (International journal of molecular sciences · 2026
    Article
  17. Article
  18. Efficacy and safety of romosozumab in patients with chronic kidney disease and osteoporosis: a narrative review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Review
  19. Article
  20. Targeting NOTCH3 to eradicate dormant and therapy-resistant multiple myeloma cells.Journal of experimental & clinical cancer research : CR · 2026
    Article

174 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

3 authors at 3 institutions in 1 country.

Jesus Delgado-CalleDepartment of Anatomy and Cell Biology, Indianapolis, IN, United States; Roudebush Veterans Administration Medical Center, Indianapolis, IN, United States. Electronic address: jedelgad@iupui.edu.
Amy Y SatoDepartment of Anatomy and Cell Biology, Indianapolis, IN, United States. Electronic address: aysato@iupui.edu.
Teresita BellidoDepartment of Anatomy and Cell Biology, Indianapolis, IN, United States; Department of Medicine, Division of Endocrinology, Indiana University School of Medicine, Indianapolis, IN, United States; Roudebush Veterans Administration Medical Center, Indianapolis, IN, United States. Electronic address: tbellido@iupui.edu.
Indiana University – Purdue University Indianapolis · USRichard L. Roudebush VA Medical Center · USUniversity of Indianapolis · US

Funding

Comprehensive Training Program in Musculoskeletal ResearchT32AR065971 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ALEXANDER G ROBLING · 2015 to 2026
$4.4M
Contribution of Osteocytes to the Musculoskeletal Effects of Multiple MyelomaR01CA209882 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI Teresita M. Bellido, Jesus Delgado-Calle · 2017 to 2026
$3.8M
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 BX004596NCI NIH HHS R01 CA209882NCRR NIH HHS S10 RR023710NIAMS NIH HHS R01 AR059357NIAMS NIH HHS T32 AR065971NIDDK NIH HHS R01 DK076007
6 · The paper itself

Abstract

After discovering that lack of Sost/sclerostin expression is the cause of the high bone mass human syndromes Van Buchem disease and sclerosteosis, extensive animal experimentation and clinical studies demonstrated that sclerostin plays a critical role in bone homeostasis and that its deficiency or pharmacological neutralization increases bone formation. Dysregulation of sclerostin expression also underlies the pathophysiology of skeletal disorders characterized by loss of bone mass, as well as the damaging effects of some cancers in bone. Thus, sclerostin has quickly become a promising molecular target for the treatment of osteoporosis and other skeletal diseases, and beneficial skeletal outcomes are observed in animal studies and clinical trials using neutralizing antibodies against sclerostin. However, the anabolic effect of blocking sclerostin decreases with time, bone mass accrual is also accompanied by anti-catabolic effects, and there is bone loss over time after therapy discontinuation. Further, the cellular source of sclerostin in the bone/bone marrow microenvironment under physiological and pathological conditions, the pathways that regulate sclerostin expression and the mechanisms by which sclerostin modulates the activity of osteocytes, osteoblasts, and osteoclasts remain unclear. In this review, we highlight the current knowledge on the regulation of Sost/sclerotin expression and its mechanism(s) of action, discuss novel observations regarding its role in signaling pathways activated by hormones and mechanical stimuli in bone, and propose future research needed to understand the full potential of therapeutic interventions that modulate Sost/sclerostin expression.

Indexed as

AnimalsBone and BonesBone Morphogenetic ProteinsBone ResorptionHumansOsteogenesisParathyroid HormoneWnt Signaling PathwayBone Morphogenetic ProteinsParathyroid HormoneAnabolismBone formationBone resorptionGlucocorticoidsMultiple myelomaOsteocytesPTHWnt/βcatenin signaling

Identifiers

PMID27742498
PMCPMC5328835
OpenAlexW2531652035

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.