Evidence map›Paper›PMID 23358608›Full record

ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2013

Serum extracellular secreted antagonists of the canonical Wnt/β-catenin signaling pathway in patients with Cushing's syndrome.

Z E Belaya, L Y Rozhinskaya, G A Melnichenko, A G Solodovnikov, N V Dragunova, A V Iljin, L K Dzeranova, I I Dedov

Abstract read
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In one paragraph

Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Review
  6. Metabolism and Endocrine Disorders: What Wnt Wrong?Frontiers in endocrinology · 2022
    Review
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Effects of endogenous hypercortisolism on bone mRNA and microRNA expression in humans.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2018
    Article
  15. A Role for Progesterone-Regulated sFRP4 Expression in Uterine Leiomyomas.The Journal of clinical endocrinology and metabolism · 2017
    Article
  16. Review
  17. Article
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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 2 institutions in 2 countries.

Z E BelayaThe National Research Center for Endocrinology, ul. Dmitria Uljanova, 11, Moscow 117036, Russia. jannabelaya@gmail.com
L Y Rozhinskaya
G A Melnichenko
A G Solodovnikov
N V Dragunova
A V Iljin
L K Dzeranova
I I Dedov
Endocrinology Research Center · RUUral State Medical University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledPatients with endogenous hypercortisolism have higher sclerostin, but do not differ in Dickkopf 1 (Dkk1) or secreted frizzled-related protein 1 (SFRP1) levels as compared to healthy control.

introductionEndogenous Cushing's syndrome (CS), usually affecting young and otherwise healthy patients, is a good model to validate the effects of supraphysiological levels of glucocorticoids in humans. This study evaluates circulating levels of extracellular antagonists of the Wnt/β-catenin signaling pathway (sclerostin, Dkk1, SFRP1) in patients with CS versus healthy individuals.

methodsForty patients with clinically and biochemically evident CS and 40 sex-, age-, and body mass index-matched healthy subjects provided fasting serum samples for sclerostin, SFRP1 and Dkk1, along with bone turnover markers.

resultsPatients with CS had higher sclerostin levels (34.5 (30.3-37.1) pmol/L) versus healthy individuals (29.9 (24.3-36.8) pmol/L) (p = 0.032). Differences in sclerostin were due to the lack of lower sclerostin values rather than an increase in protein levels above the upper limits of the healthy control. The odds of sclerostin levels being higher than 30 pmol/L were greater in patients with CS as compared with the odds in healthy subjects (odds ratio = 3.81 95 % confidence interval 1.45-10.02) (p = 0.01). It coexisted with suppressed bone formation and unchanged bone resorption markers. Dkk1, SFRP1 did not differ from the control group.

conclusionsOf all the tested proteins (sclerostin, Dkk1, SFRP1), only sclerostin showed a significant difference when contrasting CS with healthy subjects. Hypercortisolism might prevent the down-regulation of sclerostin. Targeting sclerostin seems to be a promising therapeutic approach to treating osteoporosis in patients with CS.

Indexed as

Adaptor Proteins, Signal TransducingAdultBiomarkersBone DensityBone Morphogenetic ProteinsCase-Control StudiesCushing SyndromeFemaleFemur NeckGenetic MarkersHumansIntercellular Signaling Peptides and ProteinsLumbar VertebraeMaleMembrane ProteinsMiddle AgedAdaptor Proteins, Signal TransducingBiomarkersBone Morphogenetic ProteinsDKK1 protein, humanGenetic MarkersIntercellular Signaling Peptides and ProteinsMembrane ProteinsOsteoprotegerinRANK LigandSecreted Frizzled-Related ProteinsSFRP1 protein, humanSOST protein, humanTNFRSF11B protein, humanTNFSF11 protein, human

Identifiers

PMID23358608
OpenAlexW2153089679

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Registered trials

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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.