Abstract: Angiogenesis is one of the important pathogenesis of endometriosis. Abnormal neovascularization in endometriosis promotes the proliferation, infiltration and migration of ectopic endometrial cells. High mobility group box 1 protein (HMGB1), as an important pro-inflammatory factor, is recently proved to contribute to angiogenesis in different tumors. HMGB1 can promote neoangiogenesis by acting directly on endothelial cells or indirect effects on endothelial cells by vascular endothelial growth factor (VEGF), which is synthesized and secreted by NF-κB-activating macrophages. In addition, HMGB1 also promotes proliferation and migration of endothelial cells by up-regulating the expression of fibroblast growth factor (FGF) and enhancing the activity as well as the affinity of integrins, promotes the secretion of platelet-derived growth factor (PDGF) and then recruits pericytes and smooth muscle cells, activating the formation of vascular tubular structure. Activates the secretion of TGF-β from endothelial cells, finally promoting the maturation of vascular network. Here we review the potential mechanism of HMGB1 underlying the influence of pro-angiogenesis in endometriosis in detail, thus providing a new therapeutic target for endometriosis.

Key words: HMGB1 protein, Endometriosis, Neovascularization, pathologic