Endometriosis at the Molecular Crossroads: Pathways, Targets, and Emerging Therapeutic Strategies

Endometriosis affects an estimated one in ten women of reproductive age and remains defined clinically by the presence of endometrial-like tissue outside the uterine cavity, yet its persistence depends on biological processes that extend well beyond estrogen exposure. This review argues that endometriosis is best understood as a set of molecularly heterogeneous, interconnected disease processes, hormonal, immune, vascular, epigenetic, and metabolic, that converge on a compact set of intracellular signaling nodes rather than as a single hormonal disorder. These convergence points are mapped onto candidate therapeutic targets spanning established, investigational, and preclinical stages of development, and onto biomarker strategies organized here by clinical application, diagnosis, disease stratification, prognosis, and treatment monitoring, rather than by sample source alone. Translational obstacles, including the limited predictive value of current animal models, the recurring disconnect between preclinical and clinical results, and the distinction between symptom control and disease modification, are addressed throughout rather than confined to a single closing section. Endometriosis management continues to rely on symptomatic hormonal suppression; treatment strategies grounded in the disease's molecular heterogeneity, rather than a uniform hormonal model, appear to offer the most realistic path toward durable, individualized management.