Abstract: Endometriosis is a common estrogen-dependent gynaecological disease. In addition to the well-known endocrine mechanism，secretion of steroid hormones and cytokines by endometriotic cells is associated with the pathogenesis of endometriosis. Aromatase shows higher expression in endometriosis compared with normal endometrium. Aromatase expression in ectopic endometrium is regulated by various cytokines，such as prostaglandin E2（PGE2），steroidogenic factor 1（SF-1），interleukin 6 （IL-6） and so on. Immune and environmental factors can also stimulate aromatase expression and consequently increase estradiol biosynthesis in endometriotic tissue. Additionally，the decreased expressions of 17β-hydroxysteroid dehydrogenase （17beta-HSD） type 2 and sulfate transferase in endometriotic tissues result in the reduced deactivation of E2. In summary，high E2 production and low E2 deactivation may stimulate the growth of endometriotic lesions.

Key words: Endometriosis, Estrogens, Receptors, estrogen, Aromatase