ArticleCellular and molecular life sciences : CMLS2026
Tet methylcytosine dioxygenase 2(TET2)-dependent epigenetic regulation in the pathogenesis of polycystic ovary syndrome.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- The organelle oxidative-inflammatory network in polycystic ovary syndrome: from subcellular intercellular cascades to systemic comorbidities.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder and a major cause of female infertility. While epigenetic dysregulation, notably DNA methylation, has been recognized as a key driver of PCOS pathogenesis, the specific involvement of active demethylation mediated by Ten-Eleven Translocation (TET) enzymes in the onset of the disease is currently poorly understood. In order to explore the role of TET2-mediated 5-hydroxymethylcytosine (5hmC) modifications and the underlying molecular drivers of PCOS, genome-wide 5hmC profiling was utilized to analyze granulosa cells from both PCOS patients and normal controls. Higher global 5hmC levels and TET2 expression were found in the granulosa cells of PCOS patients. Through integrated analysis, significant alterations in 5hmC at specific genomic loci were revealed, which were enriched in pathways related to MAPK signaling, gap junction communication, and oocyte meiosis. Furthermore, USP45 was identified as a downstream target of TET2 via ChIP-seq analysis. Functional experiments demonstrated that TET2 drives the overactivation of autophagic flux under hyperandrogenic conditions by stabilizing PRKAA1 via USP45-mediated deubiquitination. Conversely, pharmacological inhibition of TET2 effectively rescued these autophagic abnormalities. TET2-mediated 5hmC modification is revealed by this study as a key driver of PCOS pathogenesis; these insights offer a novel epigenetic framework for the development of PCOS therapies.
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Registered trials
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