{"paper_id":"365b4125-278a-4d4e-b9fd-8feea709987d","body_text":"Updates on the etiopathogenic mechanisms that promote endometriosis-associated infertility: a literature review\nDOI:\nhttps://doi.org/10.33448/rsd-v12i5.41462Keywords:\nEndometriosis, Infertility, Etiology, Pathology.Abstract\nIntroduction: Today, it is known that endometriosis is a chronic gynecological disease, of an inflammatory nature, marked by the presence of endometrial tissue outside the uterus (ectopic), dependent on estrogen. Endometriosis can be classified as superficial, ovarian and deep, in addition to extrapelvic and is mainly marked by dyspareunia, dysmenorrhea, dysuria, dyschezia and infertility (a challenge for 30 to 50% of these women). Objective: To identify the etiopathogenic mechanisms that could explain the prevalence of infertility in women with endometriosis. Materials and Methods: This is an integrative literature review about the new evidence that justifies infertility in women with endometriosis. The PICO strategy was used to prepare the guiding question. In addition, the descriptors “endometriosis”, “infertility”, “pathogenesis” and “etiology” were crossed in the databases National Library of Medicine (PubMed MEDLINE), Scientific Electronic Library Online (SCIELO), Google Scholar and Biblioteca Virtual Health (VHL). Results and Discussion: The environment provided by endometriosis promotes several changes, including: the high inflammatory character, cytokine imbalance, oxidative stress and changes in follicular and peritoneal fluid. The immune system seems to be impaired, with changes in the function of most immune cells. Hormonal imbalance, genetic and epigenetic factors are also fundamental. Conclusion: The association between infertility and endometriosis seems to impair conception due to changes in follicular fluid and folliculogenesis, reduced oocyte quality, changes in implantation window, sperm changes and ciliary cell dysfunction.\nReferences\nBedaiwy M. A. (2022). Endometrial cytokines, endometriosis and infertility: a deeper dive into the endometrial immune microenvironment. Fertility and sterility, 117(3), 641–642. https://doi.org/10.1016/j.fertnstert.2022.01.023\nBonavina, G., & Taylor, H. S. (2022). Endometriosis-associated infertility: From pathophysiology to tailored treatment. Frontiers in endocrinology, 13, 1020827. https://doi.org/10.3389/fendo.2022.1020827\nBroi, M. G. D., Ferriani, R. A., & Navarro, P. A. (2019). Ethiopathogenic mechanisms of endometriosis-related infertility. JBRA assisted reproduction, 23(3), 273–280. https://doi.org/10.5935/1518-0557.20190029\nCardoso, J. K, Machado, D. E., Silva, M. C., Berardo, P. T., Ferrari, R., Abrão, M. 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American journal of reproductive immunology (New York, N.Y: 1989), 85(3), e13384. https://doi.org/10.1111/aji.13384\nDownloads\nPublished\nIssue\nSection\nLicense\nCopyright (c) 2023 Beatriz Tassi Coutinho; Lívia Paiva Ferreira; Márcio José Rosa Requeijo\nThis work is licensed under a Creative Commons Attribution 4.0 International License.\nAuthors who publish with this journal agree to the following terms:\n1) Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.\n2) Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.\n3) Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work.","source_license":"CC0","license_restricted":false}