ArticleFrontiers in endocrinology2022
Androgen Excess Induced Mitochondrial Abnormality in Ovarian Granulosa Cells in a Rat Model of Polycystic Ovary Syndrome.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Redox biology in PCOS: Biomarkers, mechanistic networks, and targeted interventions (Review).International journal of molecular medicine · 2026Review
- A Biological Disease-Staging Model of Polyendocrine Metabolic Ovarian Syndrome: From Plasticity-Dominant States to Pathological Remodeling.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Bioinformatics, Machine Learning and Functional Validation Reveal Mitophagy-Related FABP5 and HMOX1 as Diagnostic and Therapeutic Targets in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- IL-22/IL-22R signaling attenuates mitochondrial damage in PCOS by modulating granulosa cell lipid metabolism through ETS1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Exploring biomarkers of mitochondrial dynamics in polycystic ovary syndrome and the effect of mesenchymal stem cell transplantation on ovarian mitochondria.Journal of ovarian research · 2026Article
- Androgen and glucocorticoid crosstalk in granulosa cells: molecular insights into polyendocrine metabolic ovarian syndrome.Frontiers in endocrinology · 2026Review
- Redox-endocrine triad in PCOS: can vitamin D, myo-inositol, and melatonin synergize as bioactive cocktails?Frontiers in endocrinology · 2026Review
- Estradiol and dihydrotestosterone exert sex-specific effects on human fibroblast and endothelial proliferation, bioenergetics, and vasculogenesis.Communications biology · 2025Article
- The role of mitochondrial dysfunction in ovarian granulosa cells in polycystic ovary syndrome.Endocrine connections · 2025Review
- Oxidative stress and energy metabolism abnormalities in polycystic ovary syndrome: from mechanisms to therapeutic strategies.Reproductive biology and endocrinology : RB&E · 2024Review
- New insights on mitochondrial heteroplasmy observed in ovarian diseases.Journal of advanced research · 2024Review
- Granulosa cell insight: unraveling the potential of menstrual blood-derived stem cells and their exosomes on mitochondrial mechanisms in polycystic ovary syndrome (PCOS).Journal of ovarian research · 2024Article
- Administration of adipose-derived mesenchymal stem cell conditioned medium improves ovarian function in polycystic ovary syndrome rats: involvement of epigenetic modifiers system.Journal of ovarian research · 2023Article
- Current Advances in Cellular Approaches for Pathophysiology and Treatment of Polycystic Ovary Syndrome.Cells · 2023Review
- Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology.International journal of molecular sciences · 2023Review
- Regulation of SIRT1 in Ovarian Function: PCOS Treatment.Current issues in molecular biology · 2023Review
- Oviductal extracellular vesicles from women with endometriosis impair embryo development.Frontiers in endocrinology · 2023Article
- Mating modifies the expression of crucial oxidative-reductive transcripts in the pig oviductal sperm reservoir: is the female ensuring sperm survival?Frontiers in endocrinology · 2023Article
- Advances in mitochondria-centered mechanism behind the roles of androgens and androgen receptor in the regulation of glucose and lipid metabolism.Frontiers in endocrinology · 2023Review
- Unveiling Therapeutic Potential of Yoga Mitigating Oxidative Stress and Mitochondrial Dysfunction in PCOS: A Randomized Controlled Trial.International journal of yogaArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Androgen excess could profoundly lead to follicular dysplasia or atresia, and finally result in polycystic ovary syndrome (PCOS); however, the exact mechanism remains to be fully elucidated. Methods: PCOS model rats were induced by dehydroepiandrosterone, and their fertility was assessed. The ovarian granulosa cells (GCs) from matured follicles of PCOS model rats were collected and identified by immunofluorescence. The mitochondrial ultrastructure was observed by transmission electron microscope and the mitochondrial function was determined by detecting the adenosine triphosphate (ATP) content and Results: The PCOS model rats were successfully induced, and their reproductive outcomes were obviously adverse. The GCs layer of the ovarian was apparently cut down and the mitochondrial ultrastructure of ovarian GCs was distinctly destroyed. The ATP content and Conclusions: Androgen excess could damage mitochondrial ultrastructure and function of GCs in rat ovary by down-regulating expression of
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