ArticleReproductive sciences (Thousand Oaks, Calif.)2017
Prenatal Exposure to Endocrine Disruptors: A Developmental Etiology for Polycystic Ovary Syndrome.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- Prenatal maternal stress is associated with alterations in the structural integrity of the hypothalamic-pituitary-gonadal axis 20 years later: Project Ice Storm.Human reproduction (Oxford, England) · 2026Article
- Polycystic ovary syndrome and idiopathic central precocious puberty: two sides of the same coin?Endocrine · 2025Review
- Research mechanism of DBP and DEHP in the development of PCOS based on network toxicology and molecular docking.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Associations of maternal per- and polyfluoroalkyl substance plasma concentrations during pregnancy with offspring polycystic ovary syndrome and related characteristics in project viva.Environmental research · 2025Article
- Bisphenol a downregulates GLUT4 expression by activating aryl hydrocarbon receptor to exacerbate polycystic ovary syndrome.Cell communication and signaling : CCS · 2024Article
- Induced Pluripotent Stem Cells as a Possible Approach for Exploring the Pathophysiology of Polycystic Ovary Syndrome (PCOS).Stem cell reviews and reports · 2024Review
- A review of nitric oxide and oxidative stress in typical ovulatory women and in the pathogenesis of ovulatory dysfunction in PCOS.Reproductive biology and endocrinology : RB&E · 2023Review
- Developmental programming: Impact of preconceptional and gestational exposure to a real-life environmental chemical mixture on maternal steroid, cytokine and oxidative stress milieus in sheep.The Science of the total environment · 2023Article
- Pathophysiological Effects of Contemporary Lifestyle on Evolutionary-Conserved Survival Mechanisms in Polycystic Ovary Syndrome.Life (Basel, Switzerland) · 2023Review
- Polycystic Ovary Syndrome and Endocrine Disruptors (Bisphenols, Parabens, and Triclosan)-A Systematic Review.Life (Basel, Switzerland) · 2023Review
- Dysfunctional Ovarian Stem Cells Due to Neonatal Endocrine Disruption Result in PCOS and Ovarian Insufficiency in Adult Mice.Stem cell reviews and reports · 2022Article
- Association of SNPs in the FK-506 binding protein (FKBP5) gene among Han Chinese women with polycystic ovary syndrome.BMC medical genomics · 2022Article
- Bisphenol A correlates with fewer retrieved oocytes in women with tubal factor infertility.Hormones (Athens, Greece) · 2022Article
- Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment.International journal of environmental research and public health · 2022Review
- Bisphenol A and its effects on the systemic organs of children.European journal of pediatrics · 2021Review
- Associations of Maternal Androgen-Related Conditions With Risk of Autism Spectrum Disorder in Progeny and Mediation by Cardiovascular, Metabolic, and Fertility Factors.American journal of epidemiology · 2021Article
- Resistance to the Insulin and Elevated Level of Androgen: A Major Cause of Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Review
- Development and validation of a liquid chromatography-tandem mass spectrometry method for the simultaneous determination of phthalates and bisphenol a in serum, urine and follicular fluid.Clinical mass spectrometry (Del Mar, Calif.) · 2020Article
- In Search of New Therapeutics-Molecular Aspects of the PCOS Pathophysiology: Genetics, Hormones, Metabolism and Beyond.International journal of molecular sciences · 2020Review
- Bisphenol A: an emerging threat to female fertility.Reproductive biology and endocrinology : RB&E · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is one of the most common and complex endocrinopathies among reproductive-age women. Polycystic ovary syndrome is characterized by symptomatology of oligomenorrhea and androgen excess, with or without presence of polycystic ovarian morphology. The etiology of PCOS is multifactorial, including genetic and environmental components. It has been previously established that prenatal androgen exposure results in a PCOS phenotype in experimental animal models and epidemiologic human studies. Investigators hypothesize that prenatal exposure to endocrine-disrupting chemicals (EDCs) may contribute to PCOS development. This review examines the emerging research investigating prenatal exposure to 3 major classes of EDCs-bisphenol A (BPA), phthalates, and androgenic EDCs-and the development of PCOS and/or PCOS-related abnormalities in humans and animal models. Highlights of this review are as follows: (1) In rodent studies, maternal BPA exposure alters postnatal development and sexual maturation;, (2) gestational exposure to dibutyl phthalate and di(2-ethylhexyl)phthalate results in polycystic ovaries and a hormonal profile similar to PCOS; and (3) androgenic EDCs, nicotine and 3,4,4'-trichlorocarbanilide, create a hyperandrogenic fetal environment and may pose a potential concern. In summary, prenatal exposure to EDCs may contribute to the altered fetal programming hypothesis and explain the significant variability in severity and presentation.
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Registered trials
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.