Endometriosis is a common gynecological disorder affecting 5–10% of women of reproductive age, characterized by endometrial-like tissue outside the uterus, causing chronic pelvic pain and infertility. It is often underdiagnosed, with a delay of up to 9 years between symptom onset and diagnosis. The disease is associated with various theories on its origin, including retrograde menstruation, coelomic metaplasia, embryonic rest, vascular/lymphatic metastasis, tissue injury and repair, denervation-reinnervation, stem cell, and genetic/epigenetic mechanisms. Endometriosis is an estrogen-dependent, fibrotic condition with complex pathophysiology involving hormonal dysregulation, inflammatory responses, immune dysregulation, and fibrosis. Estrogen dominance and progesterone resistance are key factors in its development. The disease is associated with a proinflammatory environment, involving immune cells like T cells, macrophages, dendritic cells, and uNK cells, as well as cytokines such as IL-6, IL-8, IL-1, TNF-α, and TGF-β. These factors contribute to fibrosis, scarring, and the progression of the disease. Endometriosis is also linked to infertility, with factors such as altered endometrial receptivity, impaired implantation, and disrupted folliculogenesis playing a role. MicroRNAs, such as miR-29c, miR-451, and miR-210, have been implicated in the pathophysiology of endometriosis, influencing processes like progesterone resistance, inflammation, cell proliferation, and angiogenesis. Current treatment options include surgical intervention, imaging, and emerging therapies targeting miRNAs and inflammatory pathways. The role of animal models in understanding endometriosis pathology is also significant. Despite advances, the exact mechanisms and effective treatments for endometriosis remain areas of ongoing research.Endometriosis is a common gynecological disorder affecting 5–10% of women of reproductive age, characterized by endometrial-like tissue outside the uterus, causing chronic pelvic pain and infertility. It is often underdiagnosed, with a delay of up to 9 years between symptom onset and diagnosis. The disease is associated with various theories on its origin, including retrograde menstruation, coelomic metaplasia, embryonic rest, vascular/lymphatic metastasis, tissue injury and repair, denervation-reinnervation, stem cell, and genetic/epigenetic mechanisms. Endometriosis is an estrogen-dependent, fibrotic condition with complex pathophysiology involving hormonal dysregulation, inflammatory responses, immune dysregulation, and fibrosis. Estrogen dominance and progesterone resistance are key factors in its development. The disease is associated with a proinflammatory environment, involving immune cells like T cells, macrophages, dendritic cells, and uNK cells, as well as cytokines such as IL-6, IL-8, IL-1, TNF-α, and TGF-β. These factors contribute to fibrosis, scarring, and the progression of the disease. Endometriosis is also linked to infertility, with factors such as altered endometrial receptivity, impaired implantation, and disrupted folliculogenesis playing a role. MicroRNAs, such as miR-29c, miR-451, and miR-210, have been implicated in the pathophysiology of endometriosis, influencing processes like progesterone resistance, inflammation, cell proliferation, and angiogenesis. Current treatment options include surgical intervention, imaging, and emerging therapies targeting miRNAs and inflammatory pathways. The role of animal models in understanding endometriosis pathology is also significant. Despite advances, the exact mechanisms and effective treatments for endometriosis remain areas of ongoing research.