Abstract: Endometriosis (EMs) has become a global public health problem that affects about 30%-50% of childbearing age women in the world. Neonatal angiogenesis is a prerequisite for the formation of endometriosis. CD146 not only involved in inflammation regulation, recent studies have found that CD146 also involved in tumor neovascularization. Studies have shown that EMs in ectopic lesions of CD146 increased expression of healthy endometrium, suggesting that CD146 may be involved in the development of EMs, but the exact mechanism is unclear. In terms of neovascularization, abnormal expression of CD146 may play an important role in the development of EMs. Expression of CD146 on the surface of mesenchymal stem cells (MSCs) can promote the differentiation of MSCs into vascular smooth muscle cells (VSMC), sCD146 binds angiomotin in EPC and up-regulates phosphorylated focal adhesion kinase (p-FAK), phosphorylated protein kinase B (p-AKT), phosphorylated stress-activated protein kinase (p-JNK) promotes endothelial cell proliferation and migration, and can also form a co-receptor with vascular endothelial growth factor receptor-2 (VEGFR-2) to enhance vascular endothelial growth factor (VEGF) -activated signal transduction to promote neovascularization. CD146 as a fibroblast growth factor (FGF) receptor to promote endothelial cell proliferation and migration; CD146 can also form a co-receptor with platelet-derived growth factor receptor-β (PDGFR-β) Receptors promote the formation of vascular tubular structures.
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Key words: Antigens, CD146, Endometriosis, Neovascularization, pathologic, Mesenchymal stem cells, Vascular endothelial growth factors