Abstract

  Endometriosis is an estrogen-dependent chronic inflammatory disease associated with substantial morbidity, including dyspareunia, dysmenorrhea, pelvic pain, multiple surgery, and infertility. This disease has a high impact on both woman’s physical and mental well-being. The etiology of endometriosis is complex and multifactorial, influenced by genetic, epigenetic, elevated reactive oxygen species (ROS), and oxidative stress. These factors have been postulated to play an essential role in endometriosis pathogenesis. The mitochondria are central in cellular inflammation and also a source of reactive oxygen species (ROS) in endometriosis. They are targets of ROS, and many different cellular signals like NFκB are activated due to Retrogate mensuration and ROS. These signaling pathways are responsible for the activation of apoptotic pathways in the cells of Immunity like JNK, Caspases, and IKK. This review defines molecular events linking, oxidative stress, and mitochondria, which lead to Mitochondrial Dysfunction and Apoptosis instability, alterations associated with endometriosis, its mechanisms, and pathways related to oxidative stress in ectopic peritoneal lesions.

Keywords: Endometriosis; ROS; Mitochondrial Dysfunction; Infertility; Oxidative Stress

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Citation

Citation: Royana Singh., et al. “The Role of Oxidative Stress and Antioxidant Effects in Female Endometriosis: A Systematic Review”. Acta Scientific Gastrointestinal Disorders 4.2 (2021): 23-32.

Copyright

Copyright: © 2021 Royana Singh., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.