ArticleJournal of medicine and life2013
The role of androgen receptor activity mediated by the CAG repeat polymorphism in the pathogenesis of PCOS.
Article in Journal of medicine and life, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05157373 (The Effect of Androgen Receptor Polymorphism on Endometrial Cancer Development, Progression, and Outcome), which is not on this map. Cited by 16 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.
The Effect of Androgen Receptor Polymorphism on Endometrial Cancer Development, Progression, and Outcome
Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Reduced CAG Repeats in the Androgen Receptor Gene May Independently Cause Polycystic Ovarian Syndrome.Current issues in molecular biology · 2026Review
- AR-mediated YBX3 suppresses oocyte meiotic resumption in polycystic ovary syndrome by attenuating Pde3A and Ccnb1 expression.Journal of ovarian research · 2026Article
- Pathophysiology of androgen-associated endothelial cell dysfunction in phenotype A polycystic ovarian syndrome revealed by iPSCs modeling.Frontiers in endocrinology · 2026Article
- Hyperandrogen-induced imbalance of FOXO4-AR regulatory loop contributes to ovulatory disorders in polycystic ovary syndrome.Molecular therapy. Nucleic acids · 2025Article
- CTBP1‑AS upregulation is associated with polycystic ovary syndrome and can be effectively downregulated by cryptotanshinone.Molecular medicine reports · 2022Article
- The Role of Genetics, Epigenetics and Lifestyle in Polycystic Ovary Syndrome Development: the State of the Art.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- A review of the hormones involved in the endocrine dysfunctions of polycystic ovary syndrome and their interactions.Frontiers in endocrinology · 2022Review
- Evaluation of CAG repeat length in the androgen receptor gene and polycystic ovary syndrome risk in Iranian women: A case-control study.International journal of reproductive biomedicine · 2021Article
- Androgen receptor gene mutations in 258 Han Chinese patients with polycystic ovary syndrome.Experimental and therapeutic medicine · 2021Article
- Resistance to the Insulin and Elevated Level of Androgen: A Major Cause of Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Review
- Up-regulated FHL2 inhibits ovulation through interacting with androgen receptor and ERK1/2 in polycystic ovary syndrome.EBioMedicine · 2020Article
- Physiological and Pathological Androgen Actions in the Ovary.Endocrinology · 2019Review
- Pathophysiological mechanisms of gonadotropins- and steroid hormones-related genes in etiology of polycystic ovary syndrome.Iranian journal of basic medical sciences · 2019Review
- Neuroendocrine androgen action is a key extraovarian mediator in the development of polycystic ovary syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- A hormone-dependent feedback-loop controls androgen receptor levels by limiting MID1, a novel translation enhancer and promoter of oncogenic signaling.Molecular cancer · 2014Article
- No Evidence that 2D:4D is Related to the Number of CAG Repeats in the Androgen Receptor Gene.Frontiers in endocrinology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS), one of the most common and complex endocrine disorders affecting up to 15 % of reproductive age women, is considered a predominantly hyperandrogenic syndrome according to the Androgen Excess Society. It is generally accepted that androgens determine the characteristic features of PCOS; in this context, a hyperactive androgen receptor (AR) at the levels of the GnRH pulse generator in the hypothalamus and at the granulosa cells in the ovary, skeletal muscle or adipocytes senses initially normal testosterone and dihydrotestosterone as biochemical hyperandrogenism and might be a crucial connection between the vicious circles of the PCOS pathogenesis. Polymorphism of the AR gene has been associated with different androgen pattern diseases. Several studies have demonstrated an association between AR with increased activity encoded by shorter CAG repeat polymorphism in the exon 1 of the AR gene and PCOS, although there are conflicting results in this field. The phenomenon is more complex because the AR activity is determined by the epigenetic effect of X chromosome inactivation (XCI). Moreover, we must evaluate the AR as a dynamic heterocomplex, with a large number of coactivators and corepressors that are essential to its function, thus mediating tissue-specific effects. In theory, any of these factors could modify the activity of AR, which likely explains the inconsistent results obtained when this activity was quantified by only the CAG polymorphism in PCOS.
Indexed as
Identifiers
23599814PMC3624640W1598075774What OpenQuestion 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 OpenQuestion graph.