Figure 2.

Molecular pathways underpinning endometriosis. Endometriotic lesions are characterized by a unique environment. The interplay between pro-inflammatory signals, pro-angiogenic signals, and a unique endocrine signature contribute to the pathogenesis of endometriosis. This schematic representation of the endometriotic lesion identifies three distinct molecular pathways that facilitate lesion growth in endometriosis. (1) Pro-inflammatory signals: increased neutrophil infiltration in the peritoneal fluid; increased macrophage populations in the peritoneal fluid and eutopic endometrium; elevated cytokine levels (IL-6, IL-8, IL-17, IL-33, TNF-a, etc.) in both the peritoneal fluid and plasma; at sites of inflammation, macrophages and mast cells drive neutrophil recruitment through the release of chemokines; impair regulatory T cells function. (2) Pro-angiogenic signals: Damage-associated molecular patterns: high-mobility group box 1, elevated IL-33 level, etc.; vascular endothelial growth factor. (3) Endocrine signals: local synthesis of oestradiol by endometriotic lesions; enhanced oestrogen receptor expression. ILs, interleukins; OR, oestrogen receptor; Treg cells, regulatory T cells; VEGF, vascular endothelial growth factor.