Affiliation:
1. Department of Gynecology and Reproductive Medicine Ms.Clinic MayOne Kashihara Japan
2. Department of Obstetrics and Gynecology Nara Medical University Kashihara Japan
3. Department of Obstetrics and Gynecology Nara Prefecture General Medical Center Nara Japan
4. Department of Medicine Kei Oushin Clinic Nishinomiya Japan
5. Department of Gynecology and Reproductive Medicine Aska Ladies Clinic Nara Japan
Abstract
AbstractBackgroundEndometriosis is a common gynecological condition, with symptoms including pain and infertility. Regurgitated endometrial cells into the peritoneal cavity encounter hypoxia and nutrient starvation. Endometriotic cells have evolved various adaptive mechanisms to survive in this inevitable condition. These adaptations include escape from apoptosis. Autophagy, a self‐degradation system, controls apoptosis during stress conditions. However, to date, the mechanisms regulating the interplay between autophagy and apoptosis are still poorly understood. In this review, we summarize the current understanding of the molecular characteristics of autophagy in endometriosis and discuss future therapeutic challenges.MethodsA search of PubMed and Google Scholar databases were used to identify relevant studies for this narrative literature review.ResultsAutophagy may be dynamically regulated through various intrinsic (e.g., PI3K/AKT/mTOR signal transduction network) and extrinsic (e.g., hypoxia and iron‐mediated oxidative stress) pathways, contributing to the development and progression of endometriosis. Upregulation of mTOR expression suppresses apoptosis via inhibiting the autophagy pathway, whereas hypoxia or excess iron often inhibits apoptosis via promoting autophagy.ConclusionEndometriotic cells may have acquired antiapoptotic mechanisms through unique intrinsic and extrinsic autophagy pathways to survive in changing environments.
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