Epithelial-mesenchymal transition links inflammation and fibrosis in the pathogenesis of endometriosis: a narrative review

Abstract

Endometriosis, a chronic inflammatory condition, is characterized by the growth of endometrial-like tissue outside the uterus, leading to debilitating pain and infertility. Although retrograde menstruation is widely accepted as a mechanism for the dissemination of endometrial cells to ectopic sites, the processes that enable their survival, invasion, and lesion formation remain incompletely understood. Epithelial-mesenchymal transition (EMT) has emerged as a potential driver, promoting cellular plasticity that supports ectopic implantation and invasion. Epithelial-mesenchymal transition is closely linked to inflammation, with transforming growth factor-β–mediated pathways playing a central role in driving these transitions. Chronic inflammation also induces fibroblast-myofibroblast transition (FMT) and smooth muscle metaplasia, processes that exacerbate fibrosis through excessive extracellular matrix deposition and fibroblast activation. These fibrotic changes worsen symptoms and contribute to disease progression. This review explores EMT and FMT as key mechanistic links between inflammation and fibrosis and discusses how targeting these pathways could offer novel therapeutic strategies to disrupt fibrotic progression, alleviate symptoms, and improve patient outcomes. Additionally, EMT and FMT markers hold promise as diagnostic tools, offering potential for earlier detection and more precise staging of endometriosis.