ReviewSeminars in reproductive medicine2024
Anti-Müllerian Hormone: A Molecular Key to Unlocking Polycystic Ovary Syndrome?
Review in Seminars in reproductive medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- AMH specifically targets neuronal AMHR2 to modulate the progression of polycystic ovary syndrome.BMC endocrine disorders · 2026Article
- Retrospective analysis of the association between anti-Müllerian hormone levels and metabolism and reproductive outcome across different PCOS phenotypes.American journal of translational research · 2026Article
- Increased Serum AMH in a Subgroup of Women with Idiopathic Hyperandrogenism: Do These Women Have PCOS?Biomedicines · 2025Article
- POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Gestational anti-Müllerian hormone and testosterone excess combined with maternal adiposity program for polycystic ovary syndrome.Reproduction (Cambridge, England) · 2025Review
- Monoclonal antibody therapy for PCOS?Cell metabolism · 2025Article
- The Role of Gene Alterations in the Pathogenesis of Polycystic Ovary Syndrome.Journal of clinical medicine · 2025Review
- Exploring Biomarkers Related to Cell Adhesion in Polycystic Ovary Syndrome Using Bioinformatics and Conducting Experimental Validation.International journal of general medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Anti-Müllerian hormone (AMH) is an important component within androgen receptor (AR)-regulated pathways governing the hyperandrogenic origin of polycystic ovary syndrome (PCOS). In women with PCOS, granulosa cell AMH overexpression in developing ovarian follicles contributes to elevated circulating AMH levels beginning at birth and continuing in adolescent daughters of PCOS women. A 6 to 7% incidence among PCOS women of gene variants coding for AMH or its receptor, AMHR2, suggests genetic contributions to AMH-related pathogenesis. Discrete gestational AMH administration to pregnant mice induces hypergonadotropic hyperandrogenic, PCOS-like female offspring with high circulating AMH levels that persist over three generations, suggesting epigenetic contributions to PCOS through developmental programming. Moreover, adult-onset, selective hyperactivation of hypothalamic neurons expressing gonadotropin-releasing hormone (GnRH) induces hypergonadotropic hyperandrogenism and PCOS-like traits in female mice. Both gestational and adult AMH inductions of PCOS-like traits are prevented by GnRH antagonist coadministration, implicating luteinizing hormone-dependent ovarian theca cell testosterone (T) action, mediated through the AR in AMH-induced pathogenesis. Interestingly, gestational or peripubertal exogenous T or dihydrotestosterone induction of PCOS-like traits in female mice, rats, sheep, and monkeys fails to elicit ovarian AMH hypersecretion; thus, AMH excess per se may lead to a distinct pathogenic contribution to hyperandrogenic PCOS origins.
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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.