Prostaglandin E2: the master of endometriosis?

被引：117

作者：

Wu, Meng-Hsing ^{[2
,3
]}

Lu, Chun-Wun ^{[1
]}

Chuang, Pei-Chin ^{[1
]}

Tsai, Shaw-Jenq ^{[1
]}

机构：

[1] Natl Cheng Kung Univ, Coll Med, Dept Physiol, Tainan 701, Taiwan

[2] Natl Cheng Kung Univ, Coll Med, Dept Obstet, Tainan 701, Taiwan

[3] Natl Cheng Kung Univ, Coll Med, Dept Gynecol, Tainan 701, Taiwan

来源：

EXPERIMENTAL BIOLOGY AND MEDICINE | 2010年 / 235卷 / 06期

关键词：

angiogenesis; endometriosis; macrophage; phagocytosis; proliferation; prostaglandin; steroidogenesis; stromal cells; ACUTE REGULATORY PROTEIN; FIBROBLAST-GROWTH-FACTOR; STEROIDOGENIC FACTOR-I; STROMAL CELLS; PERITONEAL-FLUID; MATRIX METALLOPROTEINASES; AROMATASE EXPRESSION; SCAVENGER RECEPTORS; PELVIC PAIN; CYCLOOXYGENASE-2; EXPRESSION;

D O I：

10.1258/ebm.2010.009321

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Endometriosis is the primary cause of infertility in women, with a prevalence rate ranging from 5% to 10%. Women with endometriosis suffer from symptoms such as chronic pelvic pain, dysmenorrhea and dyspareunia, which significantly reduce the quality of life. Endometriosis is a polygenic disease with a complex, multifactorial etiology. The mechanism responsible for the initiation and development of this disease remains largely unknown. Prostaglandin E-2 (PGE(2)), a versatile eicosanoid that exerts numerous physiological and pathological functions, has been implicated to play critical roles in the development of endometriosis. A growing body of evidence demonstrates that PGE(2) regulates many pathophysiological processes including cell proliferation, antiapoptosis, immune suppression and angiogenesis during the development of endometriosis. This review focuses on recent advances in cellular and molecular mechanisms triggered by PGE(2) that contribute to the pathological processes of endometriosis.

引用

页码：668 / 677

页数：10

共 107 条

[1] Prostaglandin E2 Via Steroidogenic Factor-1 Coordinately Regulates Transcription of Steroidogenic Genes Necessary for Estrogen Synthesis in Endometriosis [J].