The Interaction of PELP1 With FHL2 Contributes to Ectopic Endometrial Stromal Cell Proliferation, Angiogenesis, and Inflammation in Endometriosis

Endometriosis (EMS), a multifactorial and chronic benign gynecological disease characterized by ectopic endometrial growth, remains poorly understood in its pathogenesis. Proline, glutamic acid, leucine-rich protein 1 (PELP1), implicated in various diseases, has not been studied in EMS. Here, we investigated the functional role and molecular mechanisms of PELP1 in EMS progression. Using ectopic and eutopic endometrial tissues from EMS patients, we showed that PELP1 was significantly upregulated in ectopic lesions. Knockdown of PELP1 in primary ectopic endometrial stromal cells (Ec-ESCs) and the mouse model inhibited proliferation, angiogenesis, and inflammation. Mechanistically, PELP1 interacted with FHL2 to potentiate transcriptional activation of downstream factors, such as CCND1, CCND2, CDK6, ANG, CCL2, and MMP3. These findings demonstrate that PELP1 promotes EMS progression and highlight its potential as a novel therapeutic target.