Autophagy in endometriosis: Friend or foe?
Nov 20, 2017The Relationship of Autophagy and Endometriosis is still Puzzling.
Key Points
Highlight:
- Though there is an intimate relationship between autophagy and endometriosis, how autophagy affects endometriosis is controversial.
Importance:
- Endometriosis is a chronic disease and affects an estimated 10% of the female population of reproductive age.
- Emerging evidence has investigated that there is a close relationship between endometriosis and autophagy.
- The precise mechanism underlying autophagy in endometriosis has not been fully elucidated yet.
What's done here:
- In this minireview, authors aim to explore and summarize the possible mechanism of autophagy in endometriosis from the recent studies and discuss which may contribute to the abnormal level of autophagy in endometriosis.
Data:
- Though there is an intimate relationship between autophagy and endometriosis, the abnormal level of autophagy in endometriosis is still controversial.
- Autophagy is down-regulated in endometriosis by estrogen-dependent mTOR pathway.
- Drugs used for endometriosis treatment is involved in the enhancing of autophagy.
- Hypoxia, angiogenesis, ions channel, and iron may exert functions in autophagy in endometriosis.
Limitations:
- The exact role of autophagy in endometriosis needs to be studied in larger samples, especially in vivo studies.
- More autophagy-related proteins should be investigated.
- Using autophagy inhibitor will be able to confirm the exact role of autophagy in endometriosis better.
Lay Summary
Endometriosis is a chronic, estrogen-dependent disease and affects an estimated 10% of the female population of reproductive age. Unfortunately, the etiology of endometriosis is not clear. Recently emerging evidence shows that there is a close relationship between endometriosis and autophagy. However, the precise mechanism has not been fully elucidated yet.
This paper provides acquired findings of the connections between endometriosis and autophagy. Also, they discuss which may contribute to the abnormal level of autophagy in endometriosis.
Several papers have suggested that the autophagy is down-regulated in endometriosis. Activation of mTOR signaling pathway in endometriosis down-regulates autophagy activity. Also, CXCL12/CXCR4-mediated NF-kB over-expression possibly contributes to autophagy reduction. Also, the dienogest treatment used for endometriosis also affects the autophagy activity.
On the other hand, other studies show autophagy is up-regulated in endometriosis. p53 deletion in endometriosis contributes to autophagy up-regulation. Overexpression of OH-1 (Oxidative stress-mediated protein) and miR-210 (hypoxia responsive protein) possibly increases the level of autophagy. Besides, angiogenesis, ions channel, and iron may exert functions in autophagy in endometriosis.
"Nevertheless, all the studies mentioned above included only a handful of samples. To understand the exact role of autophagy in endometriosis, it is essential to include a large number of samples, evaluate more autophagy-related proteins, perform in vivo experiments, and also t is also critical to test autophagy inhibitors to confirm the exact role of autophagy in endometriosis" added authors from Anhui Medical University, China. The minireview published recently in the journal named "Biochemical and biophysical research communications."
Research Source: https://www.ncbi.nlm.nih.gov/pubmed/29107692
Endometriosis Autophagy mTOR miR-210