ArticleCommunications biology2023
Transcriptomic survey of key reproductive and metabolic tissues in mouse models of polycystic ovary syndrome.
Article in Communications biology, 2023. 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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Exploring the biological functions of PCOS: identifying hub androgen-related genes through bioinformatics.Frontiers in medicine · 2026Article
- Unpacking PCOS Inflammation: From Misconceptions to Immune Networks.Endocrinology · 2025Review
- Dissecting the Impact of Maternal Androgen Exposure on Developmental Programming through Targeting the Androgen Receptor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A Cross-Sectional Study of Alzheimer-Related Proteins in Women with Polycystic Ovary Syndrome.International journal of molecular sciences · 2024Article
- MS4A superfamily molecules in tumors, Alzheimer's and autoimmune diseases.Frontiers in immunology · 2024Review
- A study on the immunological vitality of an inflammatory biomarker explored with rs5743708 polymorphism inSaudi journal of biological sciences · 2023Article
- Androgen excess: a hallmark of polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
Corrections and comments
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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
Excessive androgen production and obesity are key to polycystic ovary syndrome (PCOS) pathogenesis. Prenatal androgenized (PNA), peripubertal androgenized, and overexpression of nerve growth factor in theca cells (17NF) are commonly used PCOS-like mouse models and diet-induced maternal obesity model is often included for comparsion. To reveal the molecular features of these models, we have performed transcriptome survey of the hypothalamus, adipose tissue, ovary and metaphase II (MII) oocytes. The largest number of differentially expressed genes (DEGs) is found in the ovaries of 17NF and in the adipose tissues of peripubertal androgenized models. In contrast, hypothalamus is most affected in PNA and maternal obesity models suggesting fetal programming effects. The Ms4a6e gene, membrane-spanning 4-domains subfamily A member 6E, a DEG identified in the adipose tissue in all mouse models is also differently expressed in adipose tissue of women with PCOS, highlighting a conserved disease function. Our comprehensive transcriptomic profiling of key target tissues involved in PCOS pathology highlights the effects of developmental windows for androgen exposure and maternal obesity, and provides unique resource to investigate molecular mechanisms underlying PCOS pathogenesis.
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What 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.