oxLDL promotes EMS-induced angiogenesis by up-regulating VEGF-A expression and secretion of endometrial cells

Abstract Background Endometriosis (EMS) is a "tumor-like" gynecological disease with distant metastasis, and studies have shown that EMS can carry out distant metastasis through vascular vessels, but the driving factor and its mechanism is not clear. Methods We use EMS animal model and gene knockout technique to explore the role of EMS-induced angiogenesis in EMS metastasis in vivo and in vitro, and clarify the role and molecular mechanism of oxLDL in promoting EMS induced angiogenesis. Results We found that microvascular density (MVD) in metastasized ectopic endometrium and eutopic endometrial tissue were higher than the normal endometrial tissue, and the plasma oxLDL was positively correlated with the distant metastasis of EMS. Furthermore, we clarify that oxLDL enhanced the MVD of endometrial tissue by up-regulating the VEGF-A expression and secretion in endometrial cells. At last, we illustrated the mechanism of oxLDL promoting the VEGF-A expression through the AKT-HIF-1α signaling pathway. Conclusion oxLDL is a risk factor promoting the EMS distant metastasis by up-regulating VEGF-A expression and secretion through AKT-HIF-1α signaling. This founding may provide theoretical support and therapeutic targets for the clinical prevention and treatment of EMS.