Evidence map›Paper›PMID 37102205›Full record

ArticleDisease models & mechanisms2023

Crosstalk between androgen receptor and WNT/β-catenin signaling causes sex-specific adrenocortical hyperplasia in mice.

Rodanthi Lyraki, Anaëlle Grabek, Amélie Tison, Lahiru Chamara Weerasinghe Arachchige, Mirko Peitzsch, Nicole Bechmann, Sameh A Youssef, Alain de Bruin, Elvira R M Bakker, Frank Claessens and 2 more

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Adrenocortical stem cells in health and disease.Nature reviews. Endocrinology · 2025
    Review
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  5. 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

12 authors at 6 institutions in 5 countries.

Rodanthi LyrakiUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.ORCID 0000-0003-4974-5567
Anaëlle GrabekUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.
Amélie TisonUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.
Lahiru Chamara Weerasinghe ArachchigeUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.ORCID 0000-0003-4492-8946
Mirko PeitzschInstitute of Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.ORCID 0000-0002-2472-675X
Nicole BechmannInstitute of Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.ORCID 0000-0002-6932-333X
Sameh A YoussefDutch Molecular Pathology Center, Department of Biomolecular Health Sciences, Faculty of Veterinary Medicine, Utrecht University, 3584 CL, Utrecht, the Netherlands.
Alain de BruinDutch Molecular Pathology Center, Department of Biomolecular Health Sciences, Faculty of Veterinary Medicine, Utrecht University, 3584 CL, Utrecht, the Netherlands.ORCID 0000-0001-8579-2649
Elvira R M BakkerDepartment of Pathology, University Medical Center Utrecht, 3508 AB, Utrecht, the Netherlands.
Frank ClaessensMolecular Endocrinology Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, 3000 Leuven, Belgium.
Marie-Christine ChaboissierUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.
Andreas SchedlUniversité Côte d'Azur, Inserm, CNRS, Institut de Biologie Valrose, 06108 Nice, France.ORCID 0000-0001-9380-7396
Centre National de la Recherche Scientifique · FRUniversity Hospital Carl Gustav Carus · DECellular Research (United States) · USJanssen (Belgium) · BEUniversity Medical Center Groningen · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Female bias is highly prevalent in conditions such as adrenal cortex hyperplasia and neoplasia, but the reasons behind this phenomenon are poorly understood. In this study, we show that overexpression of the secreted WNT agonist R-spondin 1 (RSPO1) leads to ectopic activation of WNT/β-catenin signaling and causes sex-specific adrenocortical hyperplasia in mice. Although female adrenals show ectopic proliferation, male adrenals display excessive immune system activation and cortical thinning. Using a combination of genetic manipulations and hormonal treatment, we show that gonadal androgens suppress ectopic proliferation in the adrenal cortex and determine the selective regulation of the WNT-related genes Axin2 and Wnt4. Notably, genetic removal of androgen receptor (AR) from adrenocortical cells restores the mitogenic effect of WNT/β-catenin signaling. This is the first demonstration that AR activity in the adrenal cortex determines susceptibility to canonical WNT signaling-induced hyperplasia.

Indexed as

Receptors, AndrogenWnt Signaling PathwayAnimalsbeta CateninFemaleHyperplasiaMaleMiceWnt Proteinsbeta CateninReceptors, AndrogenWnt ProteinsAdrenocortical hyperplasiaAndrogen receptorR-spondin signalingSexual dimorphism

Identifiers

PMID37102205
PMCPMC10184674
OpenAlexW4367175054

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.