ReviewReproduction (Cambridge, England)2020
Mechanisms of intergenerational transmission of polycystic ovary syndrome.
Review in Reproduction (Cambridge, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled 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.
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
51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- Bridging epigenetics and pharmacology through systematic reviews tailored to WBS methodology: the triangle decision-making model as a pioneering translational biological drug delivery system.Frontiers in medicine · 2025Pooled it
- Elevated Anti-Müllerian Hormone Levels in Newborns of Women with Polycystic Ovary Syndrome: a Systematic Review and Meta-analysis Based on Observational Studies.Reproductive sciences (Thousand Oaks, Calif.) · 2022Pooled it
- Mapping research trends of insulin resistance in polycystic ovary syndrome from 2017 to 2021: A bibliometric analysis.Frontiers in endocrinology · 2022Pooled it
- Trial
- Gestational Diabetes Mellitus and Polycystic Ovary Syndrome: A Proposed Intergenerational Metabolic Continuum Within the DOHaD Framework.Healthcare (Basel, Switzerland) · 2026Article
- Gestational lipid profile partially mediates adverse obstetric outcomes associated with polycystic ovary syndrome: a multicentre cohort study in China.Lipids in health and disease · 2026Observational
- ESR2 Regulates Granulosa Cell Proliferation and Steroidogenesis via the PI3K/AKT/mTOR Signaling Pathway in Wuding Chickens.Biology · 2026Article
- Divergent pathophysiological drivers of polycystic ovary syndrome: insulin resistance independently fuels the hyperandrogenic phenotype whilst neuroendocrine factors dominate non-hyperandrogenic presentations.Frontiers in endocrinology · 2026Article
- Amniotic-fluid metabolomics identifies phospholipid remodeling as a metabolic signature of intrauterine exposure in pregnancies with polycystic ovary syndrome.Frontiers in endocrinology · 2026Article
- On the Intimate Relationship of Adiposity to Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2025Review
- The Effect of Maternal Stress on 11beta-Hydroxysteroid Dehydrogenase Activity During Pregnancy: Evidence for Potential Pregnancy Complications and Consequences on Fetal Development and Metabolism.International journal of molecular sciences · 2025Review
- The Endocrinological Basis for Polycystic Ovary Syndrome: An Evolutionary Perspective.Endocrinology · 2025Review
- Functional and Structural Uterine Changes in PCOS.International journal of molecular sciences · 2025Review
- Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.Journal of neuroendocrinology · 2025Review
- Reduced miR-338-3p contributes to polycystic ovarian syndrome by inhibiting proliferation and enhancing apoptosis.Hereditas · 2025Article
- POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Polycystic ovary syndrome: an evolutionary metabolic adaptation.Reproduction (Cambridge, England) · 2025Review
- PCOS and Obesity: Contraception Challenges.Open access journal of contraception · 2025Review
- Induced Pluripotent Stem Cells as a Possible Approach for Exploring the Pathophysiology of Polycystic Ovary Syndrome (PCOS).Stem cell reviews and reports · 2024Review
- Effects of the prenatal and postnatal nurturing environment on the phenotype and gut microbiota of mice with polycystic ovary syndrome induced by prenatal androgen exposure: a cross-fostering study.Frontiers in cell and developmental biology · 2024Article
- An Evolutionary Model for the Ancient Origins of Polycystic Ovary Syndrome.Journal of clinical medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Developmental origins of adult disease (DoHAD) refers to critical gestational ages during human fetal development and beyond when the endocrine metabolic status of the mother can permanently program the physiology and/or morphology of the fetus, modifying its susceptibility to disease after birth. The aim of this review is to address how DoHAD plays an important role in the phenotypic expression of polycystic ovary syndrome (PCOS), the most common endocrinopathy of women characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. Clinical studies of PCOS women are integrated with findings from relevant animal models to show how intergenerational transmission of these central components of PCOS are programmed through an altered maternal endocrine-metabolic environment that adversely affects the female fetus and long-term offspring health. Prenatal testosterone treatment in monkeys and sheep have been particularly crucial in our understanding of developmental programming of PCOS because organ system differentiation in these species, as in humans, occurs during fetal life. These animal models, along with altricial rodents, produce permanent PCOS-like phenotypes variably characterized by LH hypersecretion from reduced steroid-negative feedback, hyperandrogenism, ovulatory dysfunction, increased adiposity, impaired glucose-insulin homeostasis and other metabolic abnormalities. The review concludes that DoHAD underlies the phenotypic expression of PCOS through an altered maternal endocrine-metabolic environment that can induce epigenetic modifications of fetal genetic susceptibility to PCOS after birth. It calls for improved maternal endocrine-metabolic health of PCOS women to lower their risks of pregnancy-related complications and to potentially reduce intergenerational susceptibility to PCOS and its metabolic derangements in offspring.
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What Socratic holds
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 Socratic graph.