Evidence map›Paper›PMID 32320669›Full record

ArticleCell reports2020

Beta-Catenin Causes Adrenal Hyperplasia by Blocking Zonal Transdifferentiation.

Emanuele Pignatti, Sining Leng, Yixing Yuchi, Kleiton S Borges, Nick A Guagliardo, Manasvi S Shah, Gerard Ruiz-Babot, Dulanjalee Kariyawasam, Makoto Mark Taketo, Ji Miao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

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  6. Adrenocortical stem cells in health and disease.Nature reviews. Endocrinology · 2025
    Review
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  19. Effect of Inactivation ofJournal of the Endocrine Society · 2022
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Emanuele PignattiDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Sining LengDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Division of Medical Sciences, Harvard Medical School, Boston, MA 02115, USA.
Yixing YuchiDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Kleiton S BorgesDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Nick A GuagliardoDepartment of Pharmacology, University of Virginia, Charlottesville, VA 22947, USA.
Manasvi S ShahDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Gerard Ruiz-BabotDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Dulanjalee KariyawasamDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Makoto Mark TaketoDivision of Experimental Therapeutics, Graduate School of Medicine, Kyoto University, Kyoto 606-8506, Japan.
Ji MiaoDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Paula Q BarrettDepartment of Pharmacology, University of Virginia, Charlottesville, VA 22947, USA.
Diana L CarloneDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
David T BreaultDivision of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Electronic address: david.breault@childrens.harvard.edu.
Harvard University · USBoston Children's Hospital · USUniversity of Virginia · USKyoto University · JP

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
Rosettes in Adrenal Development, Maintenance and DiseaseR01DK123694 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI David T Breault · 2019 to 2026
$5.6M
Signaling and Function of the Adrenal RosetteR01HL138241 · NHLBI · UNIVERSITY OF VIRGINIA · PI GUAGLIARDO, NICK A · 2018 to 2021
$2.1M
Regulation of the Intestinal Stem Cells During RegenerationR01DK119488 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI BREAULT, DAVID T · 2019 to 2022
$1.9M
Mechanisms of Adrenal Lineage DevelopmentR01DK100653 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI BREAULT, DAVID T · 2013 to 2016
$1.5M
Insulin Regulation of Liver X Receptor in Normal and Insulin Resistant StatesR00DK100539 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI MIAO, JI · 2016 to 2018
$747k
NHLBI NIH HHS R01 HL138241NIDDK NIH HHS P30 DK034854NIDDK NIH HHS R00 DK100539NIDDK NIH HHS R01 DK100653NIDDK NIH HHS R01 DK119488NIDDK NIH HHS R01 DK123694
6 · The paper itself

Abstract

Activating mutations in the canonical Wnt/β-catenin pathway are key drivers of hyperplasia, the gateway for tumor development. In a wide range of tissues, this occurs primarily through enhanced effects on cellular proliferation. Whether additional mechanisms contribute to β-catenin-driven hyperplasia remains unknown. The adrenal cortex is an ideal system in which to explore this question, as it undergoes hyperplasia following somatic β-catenin gain-of-function (βcat-GOF) mutations. Targeting βcat-GOF to zona Glomerulosa (zG) cells leads to a progressive hyperplastic expansion in the absence of increased proliferation. Instead, we find that hyperplasia results from a functional block in the ability of zG cells to transdifferentiate into zona Fasciculata (zF) cells. Mechanistically, zG cells demonstrate an upregulation of Pde2a, an inhibitor of zF-specific cAMP/PKA signaling. Hyperplasia is further exacerbated by trophic factor stimulation leading to organomegaly. Together, these data indicate that β-catenin drives adrenal hyperplasia through both proliferation-dependent and -independent mechanisms.

Indexed as

Adrenal Hyperplasia, CongenitalAnimalsbeta CateninCell TransdifferentiationFemaleMiceMice, Inbred C57BLMice, Knockoutbeta CateninCTNNB1 protein, mouseadrenal cortexbeta-catenincell transdifferentiationhyperplasiaWnt signaling

Identifiers

PMID32320669
PMCPMC7281829
OpenAlexW3017021618

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.