Endometriosis (EM) is characterized by the existence of endometrial mucosa outside the uterine cavity, which causesinfertility, persistent aches, and a decline in women's quality of life. Both hormone therapies and nonhormone therapies, such as NSAIDs, are ineffective, generic categories of EM drugs. Endometriosis is a benign gynecological condition, yet it shares a number of features with cancer cells, including immune evasion, survival, adhesion, invasion, and angiogenesis. Several endometriosis-related signaling pathways are comprehensively reviewed in this article, including E2, NF-κB, MAPK, ERK, PI3K/Akt/mTOR, YAP, Wnt/β-catenin, Rho/ROCK, TGF-β, VEGF, NO, iron, cytokines and chemokines. To find and develop novel medications for the treatment of EM, it is essential to implicitly determine the molecular pathways that are disordered during EM development. Additionally, research on the shared pathways between EM and tumors can provide hypotheses or suggestions for endometriosis therapeutic targets.
Keywords: Endometriosis; Pathophysiology; Pathways; Targets.
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