ReviewAmerican journal of translational research2024
Mitochondrial DNA copy number variation and gene mutations mediate polycystic ovary syndrome: research progress.
Review in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Molecular Mechanisms Underlying Reproductive Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Unraveling mitochondrial dysfunction in polycystic ovary syndrome: Pathophysiological insights.Journal of the Chinese Medical Association : JCMA · 2025Review
- The role of mitochondrial dysfunction in ovarian granulosa cells in polycystic ovary syndrome.Endocrine connections · 2025Review
- Connecting the Dots: Mitochondrial Dysfunction, PCOS, and Insulin Resistance-Insights and Therapeutic Advances.International journal of molecular sciences · 2025Review
- A Comprehensive Review of the Contribution of Mitochondrial DNA Mutations and Dysfunction in Polycystic Ovary Syndrome, Supported by Secondary Database Analysis.International journal of molecular sciences · 2025Review
- Analysis of mutations in mitochondrial transfer RNA genes and the maternal inheritance of polycystic ovary syndrome.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder affecting women of reproductive age. We provide an overview of how mitochondrial DNA (mtDNA) copy number variation (CNVs) and gene mutations mediate PCOS, including current research findings and clinical trial data to underscore a theoretical basis for further exploring its pathogenesis and developing targeted therapy. Characterized by hyperandrogenism, oligo-ovulation or anovulation, and polycystic ovarian morphology, PCOS is often accompanied by insulin resistance, metabolic syndrome, and chronic inflammation, which reduce fertility throughout the reproductive lifespan. Despite its diverse phenotypes, the etiology and pathophysiologic mechanisms of PCOS remain unclear. As the center of energy metabolism, mitochondria have emerged as a key player. Evidence suggests their structural and functional abnormalities may underlie diverse manifestations of PCOS. Previous studies have highlighted the critical role of mitochondrial morphologic alterations, functional impairments, mtDNA mutations, and CNVs in the pathogenesis and progression of PCOS. This review systematically summarizes the latest research on mtDNA CNVs and gene mutations in PCOS, identifying them as promising targets for therapeutic intervention.
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Registered trials
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