This review highlights the role of epithelial-to-mesenchymal transition in endometriosis, indicating potential therapeutic targets and diagnostic markers.
Key Points
Epithelial to mesenchymal transition in endometriosis promotes migratory and invasive cell behavior, enhancing disease severity.
Key signaling pathways, including TGF-β and PDGF, are implicated in the activation of EMT processes within ectopic lesions.
Targeting EMT in animal models has showcased regression of ectopic lesions, suggesting novel treatment pathways may be viable.
Molecular markers linked to EMT show promise as diagnostic tools, which could enhance endometriosis management strategies.