ReviewReproductive sciences (Thousand Oaks, Calif.)2023
Mitochondrial Dysfunction in Polycystic Ovary Syndrome.
Review in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- A Biological Disease-Staging Model of Polyendocrine Metabolic Ovarian Syndrome: From Plasticity-Dominant States to Pathological Remodeling.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Dietary patterns and testosterone balance: a review of clinical data and perspectives.Journal of advanced research · 2026Review
- KLaR: fusing knowledge graphs and language models for biomedical target discovery.Bioinformatics (Oxford, England) · 2026Article
- Sex Differences in Mitochondrial Function: Endocrine Regulation, Immunometabolic Signaling, and Implications for Health and Disease.International journal of molecular sciences · 2026Review
- Cardiovascular Dysfunction in Polycystic Ovary Syndrome: Mitochondrial and Inflammatory Mechanisms.BioMed research international · 2026Review
- The role of mitochondrial dysfunction in ovarian granulosa cells in polycystic ovary syndrome.Endocrine connections · 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
- Involvement of the Endocrine System is Common in Mitochondrial Disorders and Requires Long-term Comprehensive InvestigationsJournal of clinical research in pediatric endocrinology · 2024Article
- Mitochondrial Dysfunction and Risk Factors for Noncommunicable Diseases: From Basic Concepts to Future Prospective.Diseases (Basel, Switzerland) · 2024Review
- Metformin dosage and galectin-3 levels: insights from PCOS patients preparing for IVF.Frontiers in pharmacology · 2024Article
- Plasma-free metanephrines, nerve growth factor, and renalase significance in patients with PCOS.Endocrine · 2023Article
- The mutational analysis of mitochondrial DNA in maternal inheritance of polycystic ovarian syndrome.Frontiers in endocrinology · 2023Article
- Polycystic ovary syndrome due to the novel translocation 46XX t(2;9)(q21;p24).Archive of clinical cases · 2023Article
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) is a multi-causal condition. Among the genetic causes, variations in the mitochondrial DNA (mtDNA) are increasingly recognised as causative. PCOS not only occurs in known syndromic mitochondrial disorders due to pathogenic variants in the mtDNA but also in non-syndromic mitochondrial disorders. Additionally, mtDNA variants not causing a multi-system mitochondrial disorder but exclusively PCOS have been reported. Among the syndromic mitochondrial disorders, PCOS has been described in myoclonic epilepsy with ragged-red fibre (MERRF) syndrome. Among the non-syndromic mitochondrial disorders, PCOS has been described in association with insulin resistance. Several other studies suggest that mtDNA point mutations or mtDNA deletions can be associated with PCOS without manifesting in organs other than the ovaries. Evidence from animal studies suggests that function, morphology, and biogenesis of mitochondria in ovarian tissue are generally impaired in PCOS patients. In conclusion, there is increasing evidence that mtDNA variants play a pathophysiological role in the development of PCOS. Further studies are needed to establish the causal link between mtDNA variants and PCOS.
Indexed as
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What Socratic 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 Socratic graph.