Expression of smad-dependent pathway components in the pathogenesis of hyperplastic processes of the endometrium in benign uterine diseases

The results of this study demonstrate the key role of the TGF-β signaling pathway, particularly its SMAD-dependent cascade, in the pathogenesis of hyperplastic processes in the endometrium, such as polyps and hyperplasia, including their association with benign diseases of the uterine body (adenomyosis and leiomyoma). The increased expression of TGF-β and SMAD components (SMAD2, SMAD3, and SMAD4) in these conditions indicates compensatory activation of the signaling pathway in response to increased cell proliferation and impaired apoptosis. These findings underscore the complexity of regulatory mechanisms in the endometrium and the significance of the interaction between the TGF-β pathway and other molecular processes, including estrogen-dependent signaling pathway. These results support the feasibility of further investigation of TGF-β pathway components as potential diagnostic markers and therapeutic targets for the targeted treatment of endometrial hyperplastic processes. An integrated approach, including the immunohistochemical study of key markers, not only enhances diagnostics but also reduces the risk of relapse, representing an important step towards improving the quality of life for women and maintaining their reproductive health. 

Sarkisyan R.M., Gavrilova T.Yu., Asaturova A.V., Adamyan L.V. Expression of SMAD-dependent pathway components in the pathogenesis of hyperplastic processes of the endometrium in benign uterine diseases