We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
The Role of NF-κB in Endometrial Diseases in Humans and Animals: A Review.
- Authors
Zdrojkowski, Łukasz; Jasiński, Tomasz; Ferreira-Dias, Graça; Pawliński, Bartosz; Domino, Małgorzata
- Abstract
The expression of genes of various proinflammatory chemokines and cytokines is controlled, among others, by the signaling pathway of the nuclear factor kappaB (NF-κB) superfamily of proteins, providing an impact on immune system functioning. The present review addresses the influence and role of the NF-κB pathway in the development and progression of most vital endometrial diseases in human and animal species. Immune modulation by NF-κB in endometritis, endometrosis, endometriosis, and carcinoma results in changes in cell migration, proliferation, and inflammation intensity in both the stroma and epithelium. In endometrial cells, the NF-κB signaling pathway may be activated by multiple stimuli, such as bacterial parts, cytokines, or hormones binding to specific receptors. The dysregulation of the immune system in response to NF-κB involves aberrant production of chemokines and cytokines, which plays a role in endometritis, endometriosis, endometrosis, and endometrial carcinoma. However, estrogen and progesterone influence on the reproductive tract always plays a major role in its regulation. Thus, sex hormones cannot be overlooked in endometrial disease physiopathology. While immune system dysregulation seems to be NF-κB-dependent, the hormone-independent and hormone-dependent regulation of NF-κB signaling in the endometrium should be considered in future studies. Future goals in this research should be a step up into clinical trials with compounds affecting NF-κB as treatment for endometrial diseases.
- Subjects
ENDOMETRIAL diseases; ANIMAL diseases; THERAPEUTICS; IMMUNOREGULATION; GENITALIA; ENDOMETRIUM; PROGESTERONE receptors
- Publication
International Journal of Molecular Sciences, 2023, Vol 24, Issue 3, p2901
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms24032901