Cellular Phenotypic Changes in Endometriosis: Pathogenetic Mechanisms and Therapeutic Implications

Endometriosis is a common gynecological disorder characterized by extra-uterine growth of endometrial-like tissues, which causes chronic inflammation, pelvic pain and infertility and greatly impairs patients' quality of life. Despite its high prevalence, the exact pathogenesis of endometriosis remains incompletely understood and clinical therapeutic options are still limited. This paper is a combined narrative-bibliometric review. It systematically summarizes the roles and molecular mechanisms of multiple cellular phenotypic alterations including hypoxic microenvironment, aberrant cell proliferation, dysregulated autophagy, pyroptosis, ferroptosis and epithelial-mesenchymal transition (EMT) in the pathogenesis of endometriosis. Bibliometric analyses were performed based on the Web of Science Core Collection for each sub-theme, with dozens to hundreds of English-language publications included to assist in identifying research hotspots. By integrating evidence from in-vitro cellular experiments, animal models and human tissue studies, this review illustrates the interconnections among these cellular phenotypes, provides theoretical references for understanding the pathophysiology of endometriosis, and discusses corresponding translational and therapeutic implications.