The Role of mTOR and eIF Signaling in Benign Endometrial Diseases

Tatiana S Driva, Christoph Schatz, Monika Sobočan, Johannes Haybaeck
International journal of molecular sciences · 2022 · vol. 23(7) , pp. 3416 · doi:10.3390/ijms23073416 · PMID:35408777 · PMC8998789 · W4221090376
review OA: gold CC0 ⤵ 13 in-corpus citations
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This review investigates the role of mTOR and eIF signaling in benign endometrial diseases, finding mTOR overactivity promotes proliferation and invasiveness and is critical in their pathogenesis.

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Abstract

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.

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Condition tags

mesh:D004716endometriosisadenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Endometrial Hyperplasia Endometrial Hyperplasia Endometrial Hyperplasia Endometrial Hyperplasia Endometrial Hyperplasia Endometrial Hyperplasia Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometritis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (13)

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License: CC0 · commercial use OK