{"paper_id":"faf52c0c-8d53-4426-95e3-2a3e59fe07fc","body_text":"Abstract\nEndometriosis is a typical disorder affecting the female reproductive system\nand is characterized by the presence of tissue resembling the endometrium both within\nand beyond the pelvic cavity. Unfortunately, the etiology of endometriosis is not well\nunderstood. The purpose of this document is to create a summary of the factors\ncontributing to endometriosis, especially the dysregulation of cellular and molecular\npathways. Key biological processes implicated include enzyme dysregulation,\nexosome dysfunction, hormonal imbalances, apoptosis, angiogenesis, oxidative stress,\nepigenetic dysregulation, and the involvement of cytokines and chemokines. Many of\nthese factors have overlapping pathways that can enhance the survival of endometrial\ndebris and facilitate the implantation of endometrial tissue in extrauterine sites. This\nknowledge can provide a broader perspective on the onset and progression of\nendometriosis. Additionally, this study paves the way for the discovery of new\ntherapeutic targets to improve the efficacy of endometriosis treatments and reduce the\nside effects associated with current treatments. Further research is needed to better\nunderstand the underlying mechanisms that lead to the dysregulation of diseaserelated\npathways, which could ultimately be useful in early diagnosis and disease\nstaging.\nKeywords: Endometriosis, etiology, pathophysiology, dysregulation, therapeutic targets.\n11","source_license":"CC0","license_restricted":false}