The mechanism study of targeting DPP4 in regulating ferroptosis and its influence on endometrial receptivity in PCOS.

ABSTRACT:

Background

Polycystic ovary syndrome (PCOS) impairs endometrial receptivity, contributing to reproductive dysfunction. Our previous work identified ferroptosis-related dipeptidyl Peptidase 4 (DPP4) as a key regulator of endometrial receptivity in PCOS, though its mechanism remained unclear.

Objective

We aimed to explore the regulatory mechanism of DPP4 in the occurrence and tolerance of endometrial ferroptosis in PCOS.

Methods

Using high dose (HD) DHEA-induced rats and hormone-treated (E2 and HD DHEA) telomerase-immortalized human endometrial stromal cells (T-HESCs), we investigated DPP4's role in endometrial ferroptosis and receptivity. We evaluated the correlation of specific endometrial marker expression levels with reproductive outcomes.

Results

Phenotypic

SUBMITTER: Zhang J 

PROVIDER: S-EPMC12729179 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature