Pathogenesis of Endometriosis: Role of Macrophages in Endometriosis

Khaleque Newaz Khan
In: Endometriosis and Adenomyosis · 2022 · pp. 57–74 · doi:10.1007/978-3-030-97236-3_5 · W4285144301
book-chapter OA: closed CC0 ⤵ 1 in-corpus citation
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-09 ⓘ

Macrophages, influenced by ovarian steroids and LPS, mediate inflammation and promote endometriosis growth through factors like HGF, with GnRHa treatment reducing inflammation.

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

The paper reviews and synthesizes evidence on how pelvic inflammation, triggered by bacterial endotoxin (LPS) through toll-like receptor 4 (TLR4), contributes to endometriosis pathogenesis, emphasizing roles of innate immune activation. It reports that peritoneal macrophages retain estrogen and progesterone receptor encoding, and that ovarian steroids can cooperate with LPS to produce pelvic inflammatory responses that support development of endometriosis, with macrophage-driven and LPS-stimulated hepatocyte growth factor (HGF) acting as a growth-promoting factor. It also notes that treatment with the estrogen-suppressing agent GnRHa decreases local biological effects and tissue inflammation. This paper is centrally about endometriosis — it focuses on macrophages, LPS/TLR4-mediated inflammation, ovarian steroid signaling, and HGF in endometriosis pathogenesis.

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endometriosis

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last seen: 2026-06-10T17:14:06.276822+00:00
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