{"paper_id":"1072c6ea-edb8-49f1-bd1d-7602ef1c31c8","body_text":"Neuroinflammation in Endometriosis : From Peripheral Lesions to Central Pain Sensitization\nAuthors/Creators\n- 1. University of science and technology Mohammed Boudiaf\nDescription\nEndometriosis is a complex, chronic systemic condition characterized by the presence of endometrial-like tissue outside the uterine cavity, leading to chronic pelvic pain, dysmenorrhea, and infertility. Current diagnostic and therapeutic strategies remain limited due to the marked heterogeneity of endometriotic lesions—spanning superficial peritoneal implants, deep infiltrating endometriosis (DIE), and ovarian endometriomas—and their distinct cellular dynamics, such as altered aromatase activity and progesterone resistance. Crucially, surgical excision and hormonal suppression often fail to provide complete pain relief, as they target peripheral lesions rather than the underlying neurological alterations. Emerging evidence highlights that persistent peripheral inflammation and nerve fiber sprouting establish a state of central sensitization driven by spinal neuroglial adaptation. In the spinal dorsal horn, microglial M1 polarization—mediated via the CX_3CR1 / P2X_4R / NF-\\kappa B pathway—and astrocytic activation (marked by elevated GFAP) amplify neuroinflammation and central hyperexcitability. Furthermore, chronic nociceptive signaling induces structural remodeling within supraspinal sensory and limbic networks, driving affective comorbidities such as anxiety and depression. Novel non-hormonal targets, including Glycine Receptor Subunit Alpha 3 (Glra3) modulation and targeted microglial inhibition, offer promising avenues to restore neural homeostasis and alleviate chronic pelvic pain.\nFiles\nFiles\n(25.4 kB)\n| Name | Size | Download all |\n|---|---|---|\n|\nmd5:2ba9cf949d9854af439a2052a7b47bfd\n|\n25.4 kB | Download |","source_license":"CC0","license_restricted":false}