Pathogenesis of Implantation Incompetence of Endometrium in Endometriosis-Associated Infertility

Л.М. Михалева, Mekan R. Orazov, S.V. Volkova, М.Б. Хамошина, T.N. Khovanskaya, V.B. Shustova
In: Doctor.Ru · 2021 · vol. 20(6) , pp. 57–61 · doi:10.31550/1727-2378-2021-20-6-57-61 · W3202716174
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Endometriosis-associated infertility is linked to impaired endometrial receptivity due to aberrant expression of transcription factors like GATA2, GATA6, SF-1, and HOXA10.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

The paper investigates the pathogenesis of implantation incompetence by comparing endometrial receptivity in women with endometriosis-associated infertility versus other groups, using a prospective open comparative design with endometrial biopsies collected by pipelle on days 5–7 after the LH peak (the expected implantation window). It included 32 women with externally genital endometriosis (EGE) and infertility, 33 women with EGE without infertility (who had conceived within the prior 3 years), and 13 fertile controls without EGE, with immunohistochemical expression assessed for transcription factors including GATA2, GATA6, SF-1, and HOXA10. The key findings were that, in endometriosis-associated infertility, stromal expression of GATA2, GATA6, and SF-1 was increased while HOXA10 was decreased, and when compared with fertile women without EGE, increased GATA2 (stroma and glands), increased GATA6 and SF-1 (stroma), and decreased HOXA10 (stroma and glands) were observed (all reported as statistically significant). The authors conclude that impaired endometrial receptivity arises from aberrant transcription factor expression affecting local hormonal balance, though the study’s open design and biopsy-based expression measures limit inference about mechanisms beyond these molecular differences. This paper is centrally about endometriosis — it analyzes molecular determinants of endometrial implantation incompetence in women with endometriosis-associated infertility.

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Abstract

Study Objective: To expand the idea of the pathogenesis of implantation incompetence of endometrium in women with endometriosis-associated infertility. Study Design: open perspective comparative study. Materials and Methods. The study enrolled 78 women. The study group included 32 patients with endometriosis genitalis externa (EGE) and infertility; the comparison group included 33 patients with EGE who used their reproductive function not more than 3 years before the study and who were not diagnosed with infertility; the group of morphological control made 13 fertile women without EGE. The subject of the study was endometrium biopsy material obtained on day 5–7 of menstruation, following the peak blood concentration of luteinizing hormone during the expected implantation window. Study Results. When patients with endometriosis-associated infertility were compared to fertile women with EGE, we noted increased expression of GATA2 — 1.6-fold, GATA6 — 1.7-fold, SF-1 — 1.5-fold and reduced HOXA10 expression by 2.9 times (p < 0.05 in all cases) in stroma of infertile women. When patients with endometriosis-associated infertility were compared to fertile women without EGE, we recorded statistically significant (р < 0.05) increase in expression of GATA2 in stroma (2.5-fold) and glands (2.2-fold), GATA6 and SF-1 in stroma (2-fold in both cases), and reduced HOXA10 expression both in stroma (3.6-fold) and glands (2.8-fold). Conclusion. Pathogenesis of implantation incompetence of endometrium in endometriosis-associated infertility is caused by impaired endometrium receptivity because of aberrant expression of transcription factor affecting local hormonal balance. Keywords: endometriosis-associated infertility, implantation incompetence of endometrium

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