Molecular pathogenesis of ovarian endometrioma: mechanistic insights and therapeutic implications

Abstract Ovarian endometrioma (OMA), the most prevalent and clinically consequential subtype of endometriosis, represents a chronic inflammatory disorder characterized by ectopic endometrial-like lesions. This condition manifests as progressive dysmenorrhea, ovarian reserve depletion, and subfertility, imposing substantial physical and psychosocial burdens. Current diagnostic modalities remain constrained by the absence of reliable biomarkers, while surgical interventions often yield suboptimal outcomes marked by incomplete lesion resolution and elevated recurrence rates. Despite growing recognition of endometriosis as a systemic disease, the distinct pathogenic mechanisms underlying OMA formation—particularly the interplay between immune dysregulation, steroid hormone hypersensitivity, and microenvironmental reprogramming—remain insufficiently characterized. Emerging evidence implicates multifaceted pathophysiological cascades involving chronic peritoneal inflammation, T-cell polarization anomalies, vascular endothelial growth factor–mediated neoangiogenesis, progesterone resistance, and reactive oxygen species accumulation. Notably, microbiome-derived metabolites and multi-omics integration have redefined paradigms of disease progression by elucidating mechanisms sustaining lesion viability. This review consolidates recent advances in OMA pathogenesis, dissecting molecular drivers of cellular survival, adhesive interactions, and inflammatory cascades within the ovarian microenvironment.