Mechanisms of excessive estrogen formation in endometriosis
Mechanisms of excessive estrogen formation in endometriosis
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DOI：
10.1016/s0165-0378(01)00132-2
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发表时间：
2002-05-01
影响因子：
3.4
通讯作者：
Yang, SJ
中科院分区：
文献类型：
--
作者：
Bulun, SE;Gurates, B;Yang, SJ
雌激素在许多人体组织中产生，包括卵巢、胎盘和腺外部位，如脂肪组织、皮肤和大脑。芳香化酶是调节这些组织中雌激素形成的关键酶。芳香化酶活性在正常子宫内膜中检测不到。相反，芳香化酶在子宫内膜异位症中表达异常，并受到PGE的刺激（2）。这导致雌激素的局部产生，从而诱导PGE（2）形成并建立正反馈循环。子宫内膜异位症的另一种异常，即缺乏17 β-羟基类固醇脱氢酶（17 β-HSD）2型表达，损害雌二醇失活为雌酮。这些分子畸变共同促进了子宫内膜异位症中雌二醇和PGE 2数量的增加。这些发现的临床相关性通过使用芳香酶抑制剂成功治疗绝经后子宫内膜异位症的异常侵袭性病例来例证。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE(2). This results in local production of estrogen, which induces PGE(2) formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.