Evidence map›Paper›PMID 23619340›Full record

ReviewMolecular human reproduction2013

Uterine glands: development, function and experimental model systems.

Paul S Cooke, Thomas E Spencer, Frank F Bartol, Kanako Hayashi

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular human reproduction, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 211 citations in OpenAlex.

  1. Neonatal diethylstilbestrol exposure disrupts uterine epithelial apical-basal polarity and partial EMT state.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Review
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  8. Review
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  13. The Role of Adenogenesis Factors in the Pathogenesis of Endometriosis.International journal of molecular sciences · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Single-cell insights into epithelial morphogenesis in the neonatal mouse uterus.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article

35 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

4 authors at 4 institutions in 2 countries.

Paul S CookeDepartment of Physiological Sciences, University of Florida, Gainesville, FL 32610, USA. paulscooke@ufl.edu
Thomas E Spencer
Frank F Bartol
Kanako Hayashi
Auburn University · USSouthern Illinois University School of Medicine · USUniversity of Florida · USWashington State University · US

Funding

Genetic Regulation of Postnatal Uterine Morphogenesis and FunctionR21HD054679 · NICHD · TEXAS A&M UNIVERSITY · PI SPENCER, THOMAS E · 2007 to 2008
$396k
Functional Role of Wnt11 in Uterine Development and Adult FunctionR03HD058222 · NICHD · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI HAYASHI, KANAKO · 2009 to 2010
$173k
NICHD NIH HHS R03 HD058222NICHD NIH HHS R21 HD54679
6 · The paper itself

Abstract

Development of uterine glands (adenogenesis) in mammals typically begins during the early post-natal period and involves budding of nascent glands from the luminal epithelium and extensive cell proliferation in these structures as they grow into the surrounding stroma, elongate and mature. Uterine glands are essential for pregnancy, as demonstrated by the infertility that results from inhibiting the development of these glands through gene mutation or epigenetic strategies. Several genes, including forkhead box A2, beta-catenin and members of the Wnt and Hox gene families, are implicated in uterine gland development. Progestins inhibit uterine epithelial proliferation, and this has been employed as a strategy to develop a model in which progestin treatment of ewes for 8 weeks from birth produces infertile adults lacking uterine glands. More recently, mouse models have been developed in which neonatal progestin treatment was used to permanently inhibit adenogenesis and adult fertility. These studies revealed a narrow and well-defined window in which progestin treatments induced permanent infertility by impairing neonatal gland development and establishing endometrial changes that result in implantation defects. These model systems are being utilized to better understand the molecular mechanisms underlying uterine adenogenesis and endometrial function. The ability of neonatal progestin treatment in sheep and mice to produce infertility suggests that an approach of this kind may provide a contraceptive strategy with application in other species. Recent studies have defined the temporal patterns of adenogenesis in uteri of neonatal and juvenile dogs and work is underway to determine whether neonatal progestin or other steroid hormone treatments might be a viable contraceptive approach in this species.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAnimals, Newbornbeta CateninDogsFemaleHumansInfertility, FemaleMiceOrganogenesisProgestinsSheepUterusWnt Proteinsbeta CateninProgestinsWnt Proteinsadenogenesiscontraceptionendometriummurineungulate

Identifiers

PMID23619340
PMCPMC3749806
OpenAlexW2098274784

What OpenQuestion holds

Textmetadata
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.