异位子宫内膜17β-羟基类固醇脱氢酶2缺乏的分子机制
Mechanism of 17 β-hydroxysteroid dehydrogenase-2 deficiency in ectopic endometrium
Online published: 2011-04-28
李笛悠, 张 萍 . 异位子宫内膜17β-羟基类固醇脱氢酶2缺乏的分子机制[J]. 上海交通大学学报(医学版), 2011 , 31(4) : 510 . DOI: 10.3969/j.issn.1674-8115.2011.04.030
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.
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