Profilul molecular al endometrului eutopic şi ectopic în endometrioză

In: Ginecologia ro · 2020 · W3040973911
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AI-generated summary by claude@2026-06, 2026-06-08

This study characterized the molecular profile of eutopic and ectopic endometrium in endometriosis, revealing hyperestrogenism, progesterone resistance, reduced apoptosis, increased proliferation, and abnormal stem cells in ectopic lesions.

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AI-generated deep summary by claude@2026-06, 2026-06-09

This paper is a literature review characterizing the molecular profile of eutopic (uterine) and ectopic (lesional) endometrium in endometriosis, focusing on hormonal regulation, apoptosis, proliferation, and stem-cell–related changes. It summarizes findings that endometriotic implants show aromatase and 17β-HSD1 elevation with low 17β-HSD2, contributing to increased estradiol, along with progesterone resistance manifested as impaired progesterone receptor activation and failure to execute normal progesterone responses. The review also describes reduced apoptotic cell levels in eutopic endometrium (with no increase in the secretory phase versus normal endometrium), elevated Bcl-2 in peritoneal lesions, and evidence that Ki-67 proliferation correlates with disease stage and aggressiveness, while eutopic tissue stem-cell analyses report altered immunomodulatory expression and increased invasion/proliferation potential. As a narrative review, it does not provide a uniform methodology or quantify effect sizes across included studies, limiting direct comparison and generalizability. This paper is centrally about endometriosis — it synthesizes molecular/hormonal and cellular mechanisms distinguishing eutopic and ectopic endometrium in endometriosis.

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Abstract

Endometriosis represents a chronic inflammatory disease defined by the appearance of endometrial tissue outside the uterine cavity, affecting mostly reproductive-aged wo­men. Although some patients may be asymptomatic, the clinical features of endometriosis are frequently do­mi­na­ted by pelvic pain associated with infertility. Non­spe­cific symptomatology and the lack of biological scre­ening markers with increased sensitivity and specificity lead to a slow diagnostic process. The hormonal profile of the eutopic and ectopic endometrium, molecular ab­nor­ma­li­ties and enzymatic mechanisms play a key role in the etiopathogenesis of endometriosis. Endometriotic im­plants are characterized by elevated levels of aromatase and 17β-HSD1 associated with low levels of 17β-HSD2 in response to low progesterone receptors, causing an in­­creased level of estradiol. It is characteristic a status of pro­ges­te­rone resistance, described by the inability of en­do­me­trial tissue to respond adequately to progesterone, the activation failure of progesterone receptors and the use of available progesterone. Endometriosis is defined by abnormal cell proliferation of ectopic endometrial tis­sue associated with apoptosis mechanisms disorders. The level of apoptotic cells is reduced in the epithelium and stroma of the eutopic endometrium and does not in­crease at the end of the secretory phase, compared to the nor­mal endometrium. Peritoneal endometriosis le­sions as­so­ciate elevated Bcl-2 levels, while ovarian en­do­me­trio­sis shows discordant results. The correlation between Ki-67 proliferation antigen level and the disease’s stage of evo­lu­tion and aggressiveness was confirmed by nu­me­rous stu­dies. The analysis of stem cells in the eu­to­pic en­do­me­trium of patients with endometriosis showed morphological chan­ges, altered expression of im­mu­no­mo­du­la­to­ry mo­le­cules and an increased potential for invasion and pro­li­fe­ra­tion. We believe that the characterization of the bio­che­mi­cal profile of the eutopic and ectopic endometrium is a current topic of interest in the understanding of en­do­me­trio­sis, its etiopathogeny and therapeutic approach. The main molecular features of ectopic endometrium pre­sent in endometriosis lesions are characterized by hy­per­es­tro­ge­ne­mia, progesterone resistance, a reduced apoptosis ca­pa­city, an increased proliferation index, and the presence of abnormal multipotent stem cells.

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endometriosisinfertility

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