Abstract
Endometriosis (EM) is a common disease in women; however, the signaling pathways and related genes underlying the mechanisms of EM remain unclear. The present study aimed to investigate the role of angiotensin II receptor type 1 (AGTR1) in the pathogenesis of EM. Human EM tissues were collected, and the expression levels of AGTR1 and NF-κB in the tissues were analyzed using immunochemistry and western blotting, while the estrogen levels in the EM tissues were determined by ELISA. In vitro human endometrial stromal cells were used to investigate the expression levels of AGTR1 following exposure to estrogen; the interaction between AGTR1 and NF-κB was determined using reverse transcription-quantitative PCR and western blotting; and the effects of AGTR1 on cell proliferation, as well as the apoptotic and migratory abilities of the cells were evaluated using WST-1 assays, wound healing assays and flow cytometry, respectively. It was observed that both the expression levels of AGTR1 and the activity of NF-κB were increased in human EM tissues and stromal cells, and this activation of AGTR1 subsequently increased the activity of NF-κB. Moreover, estrogen was found to regulate the expression levels of AGTR1 in stromal cells. The activation of AGTR1 was demonstrated to promote cell proliferation and migration, in addition to preventing cells from undergoing apoptosis. In conclusion, the present study suggested that the increased activity of the AGTR1-NF-κB axis following the decreased exposure to estrogen may be important for the pathogenesis of EM. In addition, AGTR1 may be a potential therapeutic target for the treatment of EM.