ReviewClinical endocrinology2022
Impaired steroid hormone feedback in polycystic ovary syndrome: Evidence from preclinical models for abnormalities within central circuits controlling fertility.
Review in Clinical endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Metabolic and Anti-Inflammatory Effects of Berberine-Rationale for Its Therapeutic Potential in Polycystic Ovary Syndrome.International journal of molecular sciences · 2026Review
- A single-nucleus multiomic study of preoptic area cells in prepubertal control vs prenatally androgenized female mice.Endocrinology · 2026Article
- Bridging the Practice Gap: Polycystic Ovary Syndrome as an Under-Recognised Risk State for Ischaemic Stroke and Cardiovascular Disease.Journal of clinical medicine · 2026Review
- Farm animal models for the study of the reproductive features of polyendocrine metabolic ovarian syndrome.Frontiers in endocrinology · 2026Review
- Forebrain AR Deletion Restores PR Expression but not Reproduction in Prenatally Androgenized Female Mice.Endocrinology · 2025Article
- Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.Journal of neuroendocrinology · 2025Review
- Influence of dehydroepiandrosterone sulphate levels on the slower age-related decline in grey matter in younger women with polycystic ovary syndrome.Brain communications · 2025Article
- Exploring the Combination of Traditional Chinese and Allopathic Medicine in the Treatment of Polycystic Ovary Syndrome from the Perspective of Modern Medicine.Drug design, development and therapy · 2025Review
- Investigating GABA Neuron-Specific Androgen Receptor Knockout in two Hyperandrogenic Models of PCOS.Endocrinology · 2024Article
- [Neuroendocrine features of the pathogenesis of polycystic ovary syndrome (literature review)].Problemy endokrinologii · 2023Article
- Signaling pathways and targeted therapeutic strategies for polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
- Androgen excess: a hallmark of polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy and cause of infertility in women of reproductive age worldwide. Despite diagnostic features of anovulation, polycystic ovarian morphology, and high androgen secretion indicating the syndrome are the result of ovarian dysfunction, alterations to central neuroendocrine circuits that control reproductive capacity may drive PCOS symptoms. Resistance of gonadotrophin-releasing hormone (GnRH) neurons in the hypothalamus to inhibition by sex steroid hormone-negative feedback leads to a rapid frequency of pulsatile gonadotrophin secretion, which, in turn, drives the ovarian features of the disease. As GnRH neurons do not express steroid hormone receptors, impaired negative feedback is hypothesized to occur within an upstream network that controls GnRH pulse generation. This review will discuss the latest work from preclinical animal models of PCOS used to dissect the specific central mechanisms involved in impaired steroid hormone feedback. In particular, this review will focus on research that indicates neurons in the arcuate nucleus of the hypothalamus that express Kisspeptin, Neurokinin B and Dynorphin (KNDy cells) or γ-aminobutyric acid are targets of androgen-mediated impairment of steroid hormone feedback. Finally, this review will explore the development of therapeutic agents targeting neurons that control LH pulse frequency to resolve PCOS symptoms in the clinic.
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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.