Molecular and Cellular Changes in the Pathogenesis of Endometriosis

In: Human Physiology · 2021 · vol. 47(6) , pp. 690–699 · doi:10.1134/s0362119721060116 · W4200548694
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This review explores molecular and cellular alterations in endometriosis pathogenesis, including immune responses, hormonal changes, steroid receptor activity, and epithelial-mesenchymal transition in endometrial cells.

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This paper is a narrative review of molecular and cellular alterations implicated in endometriosis pathogenesis, focusing on evidence related to innate and adaptive immunity, disruptions in hormonal status and steroid hormone nuclear receptors, and a potential epithelial–mesenchymal transition (EMT) in endometrial cells involved in ectopic lesion establishment. It synthesizes literature suggesting that multiple interacting factors—including immune dysregulation, hormone-dependent signaling, and phenotypic changes in endometrial cells—may jointly drive ectopic focus formation. A key limitation is that the work is based on curated literature summaries rather than presenting new experimental data. This paper is centrally about endometriosis — it reviews molecular and cellular mechanisms such as immune changes, steroid receptor alterations, and EMT in ectopic lesion development.

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Abstract

The review examines molecular and cell changes in the pathogenesis of endometriosis. Literature data on innate and adaptative immunity are presented, the role of changes in the hormonal status and nuclear receptors for steroid hormones is considered, and a possible epithelial–mesenchymal transition in endometrial cells and at the site of their attachment during the formation of an ectopic focus of endometrium is discussed. The role of the combined action of various factors in the pathogenesis of endometriosis is discussed.
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Abstract

The review examines molecular and cell changes in the pathogenesis of endometriosis. Literature data on innate and adaptative immunity are presented, the role of changes in the hormonal status and nuclear receptors for steroid hormones is considered, and a possible epithelial–mesenchymal transition in endometrial cells and at the site of their attachment during the formation of an ectopic focus of endometrium is discussed. The role of the combined action of various factors in the pathogenesis of endometriosis is discussed. Similar content being viewed by others

References

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Genes linked to endometriosis by GWAS are integral to cytoskeleton regulation and suggests that mesothelial barrier homeostasis is a factor in the pathogenesis of endometriosis, Reprod. Sci., 2017, vol. 24, no. 6, p. 803. ACKNOWLEDGMENTS The authors are grateful to Maria Alexandrovna Usik for invaluable assistance in preparing the review. Funding This work was supported by Basic Research Program no. 65.4 of the Institute of Biomedical Problems, Russian Academy of Sciences (Moscow), and the Strategic Academic Leadership Program (Sechenov University, Moscow). Author information Authors and Affiliations Corresponding authors Ethics declarations COMPLIANCE WITH ETHICAL STANDARDS This article does not contain any studies involving animals or human participants performed by any of the authors. CONFLICT OF INTEREST The authors declare that they have no conflict of interests. Additional information Translated by E. Babchenko Rights and permissions About this article Cite this article Toniyan, K.A., Orlov, O.I., Boyarintsev, V.V. et al. Molecular and Cellular Changes in the Pathogenesis of Endometriosis. Hum Physiol 47, 690–699 (2021). https://doi.org/10.1134/S0362119721060116 Received: Revised: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1134/S0362119721060116

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