ArticleProceedings of the National Academy of Sciences of the United States of America2017
Neuroendocrine androgen action is a key extraovarian mediator in the development of polycystic ovary syndrome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.
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Who cites it
116 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.
- Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies.Molecular metabolism · 2020Pooled it
- Effect of metformin versus metformin plus liraglutide on gonadal and metabolic profiles in overweight patients with polycystic ovary syndrome.Frontiers in endocrinology · 2022Trial
- Canagliflozin combined with metformin versus metformin monotherapy for endocrine and metabolic profiles in overweight and obese women with polycystic ovary syndrome: A single-center, open-labeled prospective randomized controlled trial.Frontiers in endocrinology · 2022Trial
- Kisspeptin and neurokinin B interactions in modulating gonadotropin secretion in women with polycystic ovary syndrome.Human reproduction (Oxford, England) · 2020Trial
- Kisspeptin treatment induces gonadotropic responses and rescues ovulation in a subset of preclinical models and women with polycystic ovary syndrome.Human reproduction (Oxford, England) · 2019Trial
- miR-6615-3p-androgen receptor axis modulates granulosa cell fate via the MDM2-p53-BCL2 pathway in hen Prehierarchical follicles.Poultry science · 2026Article
- GnRH-receptor antagonism as a targeted approach to reproductive dysfunction in polycystic ovary syndrome.EBioMedicine · 2026Article
- VCD-induced estropause fails to enhance responsiveness to 17α-estradiol in adult female mice.GeroScience · 2026Article
- The causal relationship between polycystic ovary syndrome and structural changes in brain: a Mendelian randomization study.Brain imaging and behavior · 2026Article
- The Plasma Glycome Differences Between Women with PCOS and Healthy Controls.International journal of molecular sciences · 2026Article
- Overexpression of renin-angiotensin system peptides and receptors (OVRAS) in androgen-induced PCOS mouse ovaries.Journal of assisted reproduction and genetics · 2026Article
- Phoenixin-14 ameliorates ovarian morphology in a DHEA-induced rat model of PCOS.Reproduction & fertility · 2026Article
- Central SELENOT deficiency impairs gonadotrope axis function, sexual behavior, and fertility in male and female mice.JCI insight · 2025Article
- Hepatic KLF9 Deficiency Inhibits Dehydroepiandrosterone (DHEA)-Induced Polycystic Ovary Syndrome via Liver-Ovary Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Liver androgen receptor knockout attenuates high-fructose diet-induced glucose dysregulation in female mice.American journal of physiology. Endocrinology and metabolism · 2025Article
- Forebrain AR Deletion Restores PR Expression but not Reproduction in Prenatally Androgenized Female Mice.Endocrinology · 2025Article
- 11-Oxygenated Androgens Inhibit Brown Adipose Tissue Differentiation.Endocrinology · 2025Article
- Overexpression of androgen receptor signalling transactivator lncRNAs PRNCR1 and PCGEM1 are associated with the increased risk of PCOS.Scientific reports · 2025Article
- Unraveling the multifactorial pathophysiology of polycystic ovary syndrome: exploring lifestyle, prenatal influences, neuroendocrine dysfunction, and post-translational modifications.Molecular biology reports · 2025Review
- Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.Journal of neuroendocrinology · 2025Review
56 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is a complex hormonal disorder characterized by reproductive, endocrine, and metabolic abnormalities. As the origins of PCOS remain unknown, mechanism-based treatments are not feasible and current management relies on treatment of symptoms. Hyperandrogenism is the most consistent PCOS characteristic; however, it is unclear whether androgen excess, which is treatable, is a cause or a consequence of PCOS. As androgens mediate their actions via the androgen receptor (AR), we combined a mouse model of dihydrotestosterone (DHT)-induced PCOS with global and cell-specific AR-resistant (ARKO) mice to investigate the locus of androgen actions that mediate the development of the PCOS phenotype. Global loss of the AR reveals that AR signaling is required for all DHT-induced features of PCOS. Neuron-specific AR signaling was required for the development of dysfunctional ovulation, classic polycystic ovaries, reduced large antral follicle health, and several metabolic traits including obesity and dyslipidemia. In addition, ovariectomized ARKO hosts with wild-type ovary transplants displayed normal estrous cycles and corpora lutea, despite DHT treatment, implying extraovarian and not intraovarian AR actions are key loci of androgen action in generating the PCOS phenotype. These findings provide strong evidence that neuroendocrine genomic AR signaling is an important extraovarian mediator in the development of PCOS traits. Thus, targeting AR-driven mechanisms that initiate PCOS is a promising strategy for the development of novel treatments for PCOS.
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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.