Skip to main content
. 2023 Aug 29;37(9):e23130. doi: 10.1096/fj.202300907

FIGURE 1.

FIGURE 1

Model of pelvic endometriosis pathogenesis and pathophysiology. Origins of endometriotic lesions include transplantation of endometrial tissue fragments and cells via retrograde menstruation and coelomic metaplasia of the peritoneal mesothelium; and stem and progenitor cell differentiation. Vascular and lymphatic metastasis likely give rise to disease in extra‐pelvic sites. When superficial and deeply invasive lesions develop, they are maintained via molecular mechanisms that promote cellular adhesion cell proliferation, a localized inflammatory response, immune dysregulation, neoneuroangiogenesis, and systemic and localized steroidogenesis. Dashed arrow shows postulated effects. ER, estrogen receptor; HSD17β2, 17β‐hydroxysteroid dehydrogenase 2; ICAM, intercellular adhesion molecule; IGF, insulin‐like growth factor; NF‐κB, nuclear factor κB; NGF, nerve growth factor; PR, progesterone receptor; SF1, steroidogenic factor; STAR, steroidogenic acute regulatory protein; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor. From Ref. [3]: Zondervan KT, Becker CM, Missmer SA. Endometriosis. N Engl J Med. 2020;382(13):1244–1256. 10.1056/NEJMra1810764, with permission.