Role of Inflammation and Aromatase Expression in the Eutopic Endometrium and its Relationship with the Development of Endometriosis

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

Eutopic endometrium inflammation and increased aromatase expression promote estrogen production, supporting ectopic endometrial cell survival and peritoneal invasion, thus requiring interventions that inhibit aromatase and COX-2.

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Abstract

Epigenetic changes favoring the transcription of the aromatase gene in the endometrium allow endometrial cells to survive in ectopic locations by producing estrogens that spare them from destruction through activated macrophages. Local estrogen production hastens prostaglandin synthesis by stimulating COX-2 activity, thus creating a self-perpetuating sequence of augmented estrogen formation and enhanced inflammation. Repetitive retrograde menstruation reintroduces aromatase-positive endometrial cells endowed with the capacity to implant and invade the peritoneum. In order to control endometriosis, an effective medication must inhibit aromatase, block COX-2, decrease fibrosis and induce amenorrhea. Within this framework, progestins, either alone or in the form of oral contraceptives, appear as first-line treatment for endometriosis owing to their capacity to block enzymes such as aromatase and COX-2.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Aromatase Endometriosis Endometrium Immunity, Cellular Inflammation Aromatase Aromatase Inhibitors Aromatase Inhibitors Endometriosis Endometriosis Endometriosis Endometrium Estrogen Antagonists Estrogen Antagonists Female Humans Inflammation Inflammation Inflammation Women's Health

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References (39)

Cited by (32)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:15:58.344756+00:00
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