Evidence map›Paper›PMID 22239082›Full record

ReviewSystems biology in reproductive medicine2012

4-vinylcyclohexene diepoxide: a model chemical for ovotoxicity.

Connie J Kappeler, Patricia B Hoyer

Open access · greenAbstract readReview
In one paragraph

Review in Systems biology in reproductive medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.0field-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

60 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
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  6. Article
  7. Review
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  9. Article
  10. Review
  11. Article
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  14. An ovary-intact postmenopausal HFpEF mouse model; menopause is more than just estrogen deficiency.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Protective Role ofInternational journal of molecular sciences · 2024
    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 1 institution in 1 country.

Connie J KappelerDepartment of Physiology, College of Medicine, The University of Arizona, Tucson, AZ 85724, USA. hoyer@email.arizona.edu
Patricia B Hoyer
University of Arizona · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
SIGNALING PATHWAYS IN CHEMICAL INDUCED OVOTOXICITYR01ES009246 · NIEHS · UNIVERSITY OF ARIZONA · PI HOYER, PATRICIA B · 1999 to 2010
$2.8M
NIEHS NIH HHS ES007091NIEHS NIH HHS ES06694NIEHS NIH HHS P30 ES006694NIEHS NIH HHS R01 ES009246NIEHS NIH HHS R01 ES09246NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

The occupational chemical 4-vinylcyclohexene diepoxide (VCD) has been shown to cause selective destruction of ovarian small pre-antral (primordial and primary) follicles in rats and mice by accelerating the natural, apoptotic process of atresia. Chemicals that destroy primordial follicles are of concern to women because exposure can result in premature ovarian failure (early menopause). Initial studies using in vivo exposure of rats determined that VCD specifically targets primordial and primary (small pre-antral) follicles and that repeated dosing is required. Through a method of isolation of ovarian small follicles, biochemical and molecular studies determined that intracellular pro-apoptotic pathways are activated following VCD dosing in rats. Subsequently an in vitro system using cultured whole neonatal rat ovaries was developed to provide more mechanistic information. That approach was used to demonstrate that the cell survival c-kit/kit ligand signaling pathway is the direct target for VCD-induced ovotoxicity. Specifically, VCD directly interacts with the oocyte-associated c-kit receptor to inhibit its autophosphorylation, and thereby impair oocyte viability. The cellular and molecular approach developed to determine these findings is described in this article.

Indexed as

AnimalsApoptosisCyclohexenesDose-Response Relationship, DrugEnvironmental PollutantsFemaleHumansMiceModels, AnimalOccupational DiseasesOccupational ExposureOvarian FolliclePhosphorylationPrimary Ovarian InsufficiencyProto-Oncogene Proteins c-kitRats4-vinyl-1-cyclohexene dioxideCyclohexenesEnvironmental PollutantsProto-Oncogene Proteins c-kitVinyl Compounds

Identifiers

PMID22239082
PMCPMC3307534
OpenAlexW2166319968

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.