Details

Autor(en) / Beteiligte

• Wu, Meng‐Hsing
• Hsiao, Kuei‐Yang
• Tsai, Shaw‐Jenq

Titel

Hypoxia: The force of endometriosis

Ist Teil von

• The journal of obstetrics and gynaecology research, 2019-03, Vol.45 (3), p.532-541

Ort / Verlag

Kyoto, Japan: John Wiley & Sons Australia, Ltd

Erscheinungsjahr

2019

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• 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.