›› 2011, Vol. 31 ›› Issue (4): 510-.doi: 10.3969/j.issn.1674-8115.2011.04.030

• Review • Previous Articles     Next Articles

Mechanism of 17 β-hydroxysteroid dehydrogenase-2 deficiency in ectopic endometrium

LI Di-you, ZHANG Ping   

  1. Department of Obstetrics and Gynecology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
  • Online:2011-04-28 Published:2011-04-28


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