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. 2023 Apr 3;5:1130849. doi: 10.3389/frph.2023.1130849

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© 2023 Wang, Dragovic, Greaves, Becker and Southcombe.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The small extracellular-mediated intracellular communication in endometriosis. Small extracellular vesicles (sEVs) are present in peritoneal fluid and distinct protein profiles are shown in peritoneal sEVs from endometriosis patients compared to controls. Five proteins, peroxiredoxin-1 (PRDX1), histone H2A (H2A) type-2-C, annexin A2 (ANXA2), inter-α-trypsin inhibitor heavy chain H4 (ITIH4) and tubulin alpha-chain are solely present in peritoneal sEVs from endometriosis patients. sEVs are important intracellular communicators between different types of cells in the peritoneal microenvironment of endometriosis. One study has revealed that stromal cell-derived sEVs regulate macrophage polarisation by delivering legumain pseudogene 1 and promote angiogenesis via miR-21 and lncRNA aHIF. Additionally, stromal cell-derived sEVs promote neuro-angiogenesis. Endometrial epithelial cell sEVs inhibit lesion growth by transferring miR-30c. Peritoneal macrophages also secrete sEVs. pMΦ -derived sEVs promote lesion growth by delivering miR-22-3p and lncRNA CHL1-AS1 to stromal cells. pMΦ could potentially regulate angiogenesis, neuroangiogenesis and immune escape in endometriosis progression via sEVs. As a future potential therapeutic approach, miR-24 transfected sEVs from stromal cells are found to supress fibrosis in an endometriosis mouse model. LPS induced-macrophage-derived sEVs could attenuate endometriosis progression by repolarising pMΦ, inhibiting angiogenesis and stromal cell proliferation.