Abstract:

The apoptosis of normal endometrium is affected by estrogen. The biological activity of estrogen is mainly adjusted by 17β-hydroxysteroid dehydrogenase-2 (17β-HSD2), whose activity and quantity are dependent on progesterone that works in combination with its receptors. However, 17β-HSD2 is decreased in the ectopic endometrium of patients with endometriosis. This review is to introduce the paths how 17β-HSD2 inactivates estradiol and adjusts the growth of endometrium, and the relationship between the expression of 17β-HSD2 and the formation, gene, isoforms and function of progesterone and progesterone receptor, based on which the significance of 17β-HSD2 in the genesis, development, treatment and prognosis of endometriosis is discussed.

Key words: endometriosis, 17β-hydroxysteroid dehydrogenase-2, estrogen, progesterone, progesterone receptor, retinoic acid, metabolism