Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/ijms23073416
Keywords
mTOR signaling; eIFs; adenomyosis; endometriosis; endometritis; typical endometrial hyperplasia
Funding
- Slovenian Research Agency [J3-3069]
- Internal Research Project of the University Medical Centre Maribor [IRP 2021/01-21]
Ask authors/readers for more resources
This study investigates the role of mTOR signaling in benign endometrial diseases and highlights the overactivity of mTOR in promoting their development. Aberrant expression of the mTOR pathway is found in adenomyosis, endometriosis, and typical endometrial hyperplasia. Furthermore, derangement of mTOR signaling is linked to endometrial dysfunction caused by endometritis.
Adenomyosis, endometriosis, endometritis, and typical endometrial hyperplasia are common non-cancerous diseases of the endometrium that afflict many women with life-impacting consequences. The mammalian target of the rapamycin (mTOR) pathway interacts with estrogen signaling and is known to be dysregulated in endometrial cancer. Based on this knowledge, we attempt to investigate the role of mTOR signaling in benign endometrial diseases while focusing on how the interplay between mTOR and eukaryotic translation initiation factors (eIFs) affects their development. In fact, mTOR overactivity is apparent in adenomyosis, endometriosis, and typical endometrial hyperplasia, where it promotes endometrial cell proliferation and invasiveness. Recent data show aberrant expression of various components of the mTOR pathway in both eutopic and ectopic endometrium of patients with adenomyosis or endometriosis and in hyperplastic endometrium as well. Moreover, studies on endometritis show that derangement of mTOR signaling is linked to the establishment of endometrial dysfunction caused by chronic inflammation. This review shows that inhibition of the mTOR pathway has a promising therapeutic effect in benign endometrial conditions, concluding that mTOR signaling dysregulation plays a critical part in their pathogenesis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available