Recent insights in pathogenesis of endometriosis with focus on gut microbiota.

EMs is a chronic, estrogen-dependent systemic inflammatory disorder defined by the ectopic implantation of endometrial glands and stroma and is frequently associated with dysmenorrhea, chronic pelvic pain, infertility, and substantial impairment in quality of life. Despite its high prevalence and socioeconomic burden, the etiopathogenesis of EMs remains incompletely elucidated and appears to involve intricate interactions among endocrine dysregulation, immune dysfunction, epigenetic reprogramming, ferroptosis, miRNA-mediated gene regulation, environmental exposures, and lifestyle-related factors. Accumulating evidence has increasingly implicated GM dysbiosis in EMs development and progression. Alterations in microbial diversity and composition have been associated with changes in host immune homeostasis, estrogen metabolism, intestinal barrier integrity, inflammatory signaling cascades, microbial-derived metabolites, and gut-brain axis communication, which may foster a pro-inflammatory pelvic microenvironment that in turn may facilitate lesion implantation, angiogenesis, neuroinflammation, and pain sensitization. Elevated lipopolysaccharide levels, reduced short-chain fatty acid production, Th17/Treg imbalance, macrophage polarization, and epigenetic modulation have also been associated with GM perturbations in EMs. This review synthesizes current advances in understanding the multifactorial mechanisms underlying EMs pathogenesis, with a particular emphasis on microbiota-host interactions. We also discuss emerging microbiota-targeted therapeutic strategies, including probiotics, dietary modulation, and fecal microbiota transplantation, highlighting their translational potential as adjunctive approaches for disease management and personalized medicine in EMs.