Exploring the regulatory mechanisms of reproductive dysfunction in obese patients with PCOS

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Polycystic ovary syndrome (PCOS) is a complex endocrine disorder often worsened by obesity, leading to chronic inflammation, metabolic dysregulation, and reproductive dysfunction. This study aims to uncover the molecular mechanisms underlying reproductive dysfunction in obese PCOS patients by identifying key regulatory genes, pathways, and immune interactions, with a focus on cross-tissue regulators and potential therapeutic targets. We analyzed transcriptomic data from multiple datasets, including GSE43322, GSE43264, GSE124226, GSE54250, GSE48301, and GSE114419. Differential gene expression analysis, weighted gene co-expression network analysis, immune infiltration profiling, and pathway enrichment were performed. Cross-tissue comparisons identified overlapping genes, and molecular docking was conducted to screen FDA-approved small molecules targeting key regulators. qPCR was conducted on PBMCs from 5 PCOS patients and 5 controls to validate the expression of Cytoplasmic Polyadenylation Element Binding Protein 4 (CPEB4). CPEB4 was identified as a critical cross-tissue regulator linking systemic metabolic dysregulation with local ovarian dysfunction. It was enriched in pathways related to oocyte maturation and meiosis, highlighting its role in reproductive health. Immune infiltration analysis revealed increased pro-inflammatory M1 macrophages and decreased anti-inflammatory M2

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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