The role of the adhesion molecule Nectin-4 in the pathogenesis of endometriosis
Nectin-4 expression was significantly higher in endometriotic lesions and eutopic endometrium of endometriosis patients compared to controls, suggesting a role in endometriosis pathogenesis.
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The paper investigated whether the adhesion molecule Nectin-4 is differentially expressed in normal endometrium versus ectopic endometriotic tissues. Using immunohistochemistry, it compared Nectin-4 expression across ovarian endometriosis (n=20), peritoneal endometriosis (n=20), endometrium of endometriosis (n=20), and a control group without endometriosis (n=20). Nectin-4 expression was higher in ovarian and peritoneal endometriotic lesions than in controls, and the difference was also significant in the endometrium of patients with endometriosis. The authors’ main limitation is that the study reports comparative expression without additional mechanistic experiments to establish causality, and it does not test Nectin-4-targeted interventions. This paper is centrally about endometriosis—focusing on Nectin-4 expression as a potential contributor to endometriosis pathogenesis.
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Cited by (8)
- The Role of Cadherin 12 (CDH12) in the Peritoneal Fluid among Patients with Endometriosis and Endometriosis-Related Infertility 2022
- Ectopic Endometrial Cell-Derived Exosomal Moesin Induces Eutopic Endometrial Cell Migration, Enhances Angiogenesis and Cytosolic Inflammation in Lesions Contributes to Endometriosis Progression 2022
- A Comparative Study of Endometriosis and Normal Endometrium Based on Ultrasound Observation 2022
- Macrophage-derived netrin-1 contributes to endometriosis- associated pain 2021
- Exosomal Moesin Derives From Ectopic Stromal Cells Constructs A “Migration-Vascularization-Inflammation” Loop In Endometriosis 2021
- Macrophage-derived Netrin-1 participates in endometriosis-associated pain 2019
- Transforming growth factor β1 enhances adhesion of endometrial cells to mesothelium by regulating integrin expression 2017
- 10.1016/s0246-1064(17)65070-9 2000
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