Review

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

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  • Department of Obstetrics and Gynecology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China

Online published: 2011-04-28

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.

Cite this article

LI Di-you, ZHANG Ping . Mechanism of 17 β-hydroxysteroid dehydrogenase-2 deficiency in ectopic endometrium[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2011 , 31(4) : 510 . DOI: 10.3969/j.issn.1674-8115.2011.04.030

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