Aim: Summarize recent findings of how hypoxia regulates numerous important processes to facilitate the implantation, proliferation and progression of ectopic endometriotic lesions. Methods: Most up-to-date evidences about how hypoxia contributes to the disease pathogenesis of endometriosis and potential therapeutic approaches were collected by conducting a comprehensive search of medical literature electronic databases. Quality of data was analyzed by experienced experts including gynecologist and basic scientists. Results: Uterus is a highly vascularized organ, which makes endometrial cells constantly expose to high concentration of oxygen. When endometrial tissues shed off from the eutopic uterus and retrograde to the peritoneal cavity, they face severe hypoxic stress. Even with successful implantation to ovaries or peritoneum, the hypoxic stress remains as a critical issue because endometrial cells are used to live in the well-oxygenated environment. Under the hypoxia condition, cells undergo epigenetic modulation and evolve several survival processes including steroidogenesis, angiogenesis, inflammation and metabolic switch. The complex gene regulatory network driven by hypoxia ensures endometriotic cells can survive under the hostile peritoneal microenvironment. Conclusion: Hypoxia plays critical roles in promoting pathological processes to facilitate the development of endometriosis. Targeting hypoxia-mediated gene network represents an alternative approach for the treatment of endometriosis.
All Science Journal Classification (ASJC) codes
- Obstetrics and Gynaecology