Evidence map›Paper›PMID 27965160›Full record

ReviewBone2017

Hormonal and systemic regulation of sclerostin.

Matthew T Drake, Sundeep Khosla

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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 77 citations in OpenAlex.

  1. Trial
  2. 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
  3. Trial
  4. Article
  5. Review
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  8. Article
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  11. Advances in laboratory medicine · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

2 authors at 2 institutions in 1 country.

Matthew T DrakeDepartment of Endocrinology, Kogod Center on Aging, Mayo Clinic College of Medicine, Rochester, MN, USA. Electronic address: drake.matthew@mayo.edu.
Sundeep KhoslaDepartment of Endocrinology, Kogod Center on Aging, Mayo Clinic College of Medicine, Rochester, MN, USA.
Mayo Clinic · USWinnMed · US

Funding

SEX STEROIDS, GROWTH FACTORS, &BONE CELL FUNCTIONP01AG004875 · NIA · MAYO CLINIC ROCHESTER · PI MONROE, DAVID G · 1985 to 2019
$30.8M
EPIDEMIOLOGY OF AGE-RELATED BONE LOSS, &FRACTURESR01AR027065 · NIAMS · MAYO CLINIC ROCHESTER · PI AMIN, SHREYASEE, KHOSLA, SUNDEEP · 1986 to 2020
$14.9M
Estrogen receptor regulation of bone metabolism in adult miceR01AG048792 · NIA · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP, MONROE, DAVID G · 2015 to 2019
$1.0M
NIAMS NIH HHS R01 AR027065NIA NIH HHS P01 AG004875NIA NIH HHS R01 AG048792
6 · The paper itself

Abstract

The Wnt/β-catenin signaling pathway plays an essential role in osteoblast biology. Sclerostin is a soluble antagonist of Wnt/β-catenin signaling secreted primarily by osteocytes. Current evidence indicates that sclerostin likely functions as a local/paracrine regulator of bone metabolism rather than as an endocrine hormone. Nonetheless, circulating sclerostin levels in humans often reflect changes in the bone microenvironment, although there may be exceptions to this observation. Using existing assays, circulating sclerostin levels have been shown to be altered in response to both hormonal stimuli and across a variety of normal physiological and pathophysiological conditions. In both rodents and humans, parathyroid hormone provided either intermittently or continuously suppresses sclerostin levels. Likewise, most evidence from both human and animal studies supports a suppressive effect of estrogen on sclerostin levels. Efforts to examine non-hormonal/systemic regulation of sclerostin have in general shown less consistent findings or have provided associations rather than direct interventional information, with the exception of mechanosensory studies which have consistently demonstrated increased sclerostin levels with skeletal unloading, and conversely decreases in sclerostin with enhanced skeletal loading. Herein, we will review the existent literature on both hormonal and non-hormonal/systemic factors which have been studied for their impact on sclerostin regulation.

Indexed as

AgingAnimalsBone Morphogenetic ProteinsDiseaseHormonesHumansBone Morphogenetic ProteinsHormonesBoneDiabetesEstrogenHormoneLoadingOsteocyteParathyroidSclerostinUnloading

Identifiers

PMID27965160
PMCPMC5329134
OpenAlexW2560220756

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.