GPX4 deficiency-induced ferroptosis drives endometrial epithelial fibrosis in polycystic ovary syndrome.

ABSTRACT: The increased risk of infertility and endometrial lesions (such as endometrial hyperplasia or cancer) in polycystic ovary syndrome (PCOS) are closely associated with the lack of cyclical transformation in the endometrium. However, the underlying mechanisms remain incompletely understood. Though integrating single-cell RNA-sequencing, transcriptomics, and metabolomics analysis, we found that glutathione (GSH) metabolism disorder and the overactivation of ferroptosis, triggered by glutathione peroxidase 4 (GPX4) deficiency in endometrial epithelial cells, were the consequences of the prolonged endometrial proliferative phase in PCOS. This change may collectively contribute to some extent to decidualization failure. We further performed GSVA analysis and determined that the negative correlati

SUBMITTER: Ye Z 

PROVIDER: S-EPMC12023900 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature