Figure 10.

Model for ERβ direct response cellular pathways in ectopic lesions and eutopic endometrium. (A) Model for direct ERβ-responsive pathways in ectopic lesions driving the progression of ectopic lesions. Nuclear ERβ directly activates TNFα/NF-κB and the ROS detoxification system in shedding endometrium fragments to evade the host immune surveillance system and then enhances EMT, proliferation, and hypoxia signaling to promote endometriosis progression. (B) Model for directly ERβ-responsive pathways in the eutopic endometrium. Nuclear ERβ directly activates proliferation, UPR, and IL-6/JAK/STAT3 inhibitory signaling in the eutopic endometrium, driving endometrial dysfunction.