Abstract
Implantation of retrogradely shed endometrium during menstruation needs the acquisition of an adequate blood supply. The endometrium has angiogenic potential and endometriotic lesions grow larger in blood supply areas. Thus, angiogenesis is a prerequisite for the endometriosis development. Vascular Endothelial Growth Factor (VEGF) family is particularly important in regulating angiogenesis since anti-VEGF agents inhibit implants in animal models. Dopamine and its agonists, such as Cabergoline (Cb2), are able to promote VEGFR2 endocitosis in endothelial cells (EC), preventing VEGF-VEGFR2 binding and reducing neoangiogenesis.
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