Department of Obstetrics and Gynecology, National Cheng Kung University, Tainan 701, Taiwan, Republic of China.
Exp Biol Med (Maywood). 2010 Jun;235(6):668-77. doi: 10.1258/ebm.2010.009321.
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.
子宫内膜异位症是女性不孕的主要原因，患病率为 5%至 10%。患有子宫内膜异位症的女性会出现慢性盆腔疼痛、痛经和性交困难等症状，这会显著降低生活质量。子宫内膜异位症是一种多基因疾病，具有复杂的、多因素的病因。导致这种疾病发生和发展的机制在很大程度上仍然未知。前列腺素 E2（PGE2）是一种多功能类二十烷酸，具有多种生理和病理功能，据报道它在子宫内膜异位症的发展中起着关键作用。越来越多的证据表明，PGE2 在子宫内膜异位症的发展过程中调节许多病理生理过程，包括细胞增殖、抗凋亡、免疫抑制和血管生成。本综述重点介绍了 PGE2 引发的细胞和分子机制的最新进展，这些机制有助于子宫内膜异位症的病理过程。
