Particularități histopatologice și evaluarea imunohistochimică a procesului de invazivitate în endometrioza extragenitală
The SDF-1/CXCR4 axis plays a crucial role in the invasion and metastatic processes of many human cancers. We are interested in investigating the involvement of this axis in the development of extragenital endometriosis, given its potential to influence the invasive behavior of endometrial tissue. This research could provide new insights into disease mechanisms and identify new targets for treatment. SDF-1 and CXCR4 protein expression was evaluated by immunohistochemistry in 43 cases of endometriosis and in 6 cases of normal endometrial tissues. SDF-1 and CXCR4 proteins were expressed both in endometriosis lesions and in glandular epithelial cells and mesenchymal cells of normal endometrial tissue. Positive staining was localized to the cytoplasm. A specific value was used to calculate and analyze the intensity of immunohistochemical expression. The expressions of these two proteins in endometriosis lesions were significantly higher compared with those in normal endometrial tissues, and the differences were statistically significant (P<0.05). Both markers, SDF-1 and its receptor CXCR4, were more highly expressed in endometriosis lesions compared with normal endometrial tissue. SDF-1, through its interaction with the CXCR4 receptor, plays a significant role in the pathogenesis of endometriosis by contributing to the proliferation process of endometrial stromal cells.
Authors
- Eremei Zota (ORCID: https://orcid.org/0000-0003-1365-2633)
- Claudiu Mărgăritescu (ORCID: https://orcid.org/0000-0002-4937-5589)
- E Cazacu (ORCID: https://orcid.org/0000-0003-2893-6401)
Institutions
- University of Medicine and Pharmacy of Craiova (RO)
- Nicolae Testemițanu State University of Medicine and Pharmacy (MD)
Publication Details
- Journal
- Akademos
- Published
- 2025-04-29
- DOI
- https://doi.org/10.52673/18570461.25.1-76.07
- Primary Topic
- Endometriosis Research and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00