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Mechanistically, EMT production is associated with the pathophysiology of fibrosis through the IL-33-suppression of tumorigenicity 2 (ST2) axis, the transforming growth factor (TGF)-β signaling pathway, and the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT/glycogen synthase kinase 3 beta (GSK-3β)/β-catenin axis, which promote the migration and invasion of endometrial mesenchymal cells and mediate peritoneal adhesions (39–42)