Endometriosis: disease pathophysiology and the role of prostaglandins

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This review explores the expression, regulation, and action of prostaglandins in the cellular and molecular mechanisms contributing to the development and maintenance of endometriosis, a prevalent disease affecting women of reproductive age.

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This 2007 review examines the polygenic, multifactorial pathophysiology of endometriosis with emphasis on prostaglandins, describing how they are expressed, regulated, and act within cellular and molecular mechanisms tied to disease development and/or maintenance. It characterizes the condition’s prevalence (about 10% of women of reproductive age), key symptoms (chronic pelvic pain, dysmenorrhoea, dyspareunia), and outcomes including infertility, while noting that the initiating and promoting mechanisms remain unclear. A limitation is that it is a narrative review focused on prostaglandin biology rather than presenting new experimental data or systematically evaluating all causal pathways. This paper is centrally about endometriosis — focusing on the role of prostaglandins in endometriosis pathophysiology.

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Abstract

Endometriosis is considered to be a polygenic disease with a complex, multifactorial aetiology that affects about 10% of women in the reproductive age. Women with endometriosis have symptoms that include chronic pelvic pain, dysmenorrhoea and dyspareunia, significantly reducing their quality of life. Endometriosis is also the primary cause of infertility in women, with the prevalence rate ranging from 20% to 50%. The high prevalence and severe outcomes of this disease have made it a major public health concern in modern society. Currently, the mechanism(s) responsible for the initiation and promotion of this disease remains obscure. In this review, we focus on the expression, regulation and action of prostaglandins in the cellular and molecular mechanisms that contribute to the development and/or maintenance of endometriosis.
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Published online by Cambridge University Press: 16 January 2007 Endometriosis is considered to be a polygenic disease with a complex, multifactorial aetiology that affects about 10% of women in the reproductive age. Women with endometriosis have symptoms that include chronic pelvic pain, dysmenorrhoea and dyspareunia, significantly reducing their quality of life. Endometriosis is also the primary cause of infertility in women, with the prevalence rate ranging from 20% to 50%. The high prevalence and severe outcomes of this disease have made it a major public health concern in modern society. Currently, the mechanism(s) responsible for the initiation and promotion of this disease remains obscure. In this review, we focus on the expression, regulation and action of prostaglandins in the cellular and molecular mechanisms that contribute to the development and/or maintenance of endometriosis. - Type - Review Article - Information - Copyright - © 2007 Cambridge University Press - 70 - Cited by Cited by Crossref Citations D’Cruz, Osmond J. and Uckun, Fatih M. 2007. Targeting Mast Cells in Endometriosis with Janus Kinase 3 Inhibitor, JANEX‐1. American Journal of Reproductive Immunology, Vol. 58, Issue. 2, p. 75. Petraglia, Felice Musacchio, Concetta Luisi, Stefano and De Leo, Vincenzo 2008. Hormone-dependent gynaecological disorders: a pathophysiological perspective for appropriate treatment. Best Practice & Research Clinical Obstetrics & Gynaecology, Vol. 22, Issue. 2, p. 235. Banu, S. K. Lee, J. Speights, V. O. Starzinski-Powitz, A. and Arosh, J. A. 2008. Cyclooxygenase-2 Regulates Survival, Migration, and Invasion of Human Endometriotic Cells through Multiple Mechanisms. Endocrinology, Vol. 149, Issue. 3, p. 1180. Lundeberg, Thomas and Lund, Iréne 2008. Is There a Role for Acupuncture in Endometriosis Pain, Or ‘endometrialgia’?. Acupuncture in Medicine, Vol. 26, Issue. 2, p. 94. Hsu, Chih-Chao Lu, Chun-Wun Huang, Bu-Miin Wu, Meng-Hsing and Tsai, Shaw-Jenq 2008. Cyclic Adenosine 3′,5′-Monophosphate Response Element-Binding Protein and CCAAT/Enhancer-Binding Protein Mediate Prostaglandin E2-Induced Steroidogenic Acute Regulatory Protein Expression in Endometriotic Stromal Cells. The American Journal of Pathology, Vol. 173, Issue. 2, p. 433. Banu, Sakhila K. Lee, JeHoon Starzinski-Powitz, Anna and Arosh, Joe A. 2008. Gene expression profiles and functional characterization of human immortalized endometriotic epithelial and stromal cells. Fertility and Sterility, Vol. 90, Issue. 4, p. 972. Wu, Meng-Hsing Cheng, Yueh-Chin and Chang, Fong-Ming 2008. Ultrasonographic Assessment of Ovarian Endometrioma. Journal of Medical Ultrasound, Vol. 16, Issue. 4, p. 241. Gore, Richard M. Szucs, Richard A. Wolf, Ellen L. Scholz, Francis J. Eisenberg, Ronald L. and Rubesin, Stephen E. 2008. Textbook of Gastrointestinal Radiology. p. 1203. Kong, B Tian, Y Zhu, W Su, S and Kan, Y 2008. Effects of Celecoxib and Nimesulide on the Proliferation of Ectopic Endometrial Stromal Cells in vitro. Journal of International Medical Research, Vol. 36, Issue. 5, p. 1032. Guo, Sun-Wei 2008. Emerging drugs for endometriosis. Expert Opinion on Emerging Drugs, Vol. 13, Issue. 4, p. 547. Banu, Sakhila K. Starzinski-Powitz, Anna Speights, V.O. Burghardt, Robert C. and Arosh, Joe A. 2009. Induction of peritoneal endometriosis in nude mice with use of human immortalized endometriosis epithelial and stromal cells: a potential experimental tool to study molecular pathogenesis of endometriosis in humans. Fertility and Sterility, Vol. 91, Issue. 5, p. 2199. Templeman, Claire 2009. Adolescent Endometriosis. Obstetrics and Gynecology Clinics of North America, Vol. 36, Issue. 1, p. 177. Lousse, Jean-Christophe Defrère, Sylvie Ramos, Reinaldo González Van Langendonckt, Anne Colette, Sébastien and Donnez, Jacques 2009. Involvement of Iron, Nuclear Factor-Kappa B (NF-κB) and Prostaglandins in the Pathogenesis of Peritoneal Endometriosis-Associated Inflammation: A Review. Journal of Endometriosis, Vol. 1, Issue. 1, p. 19. Zhu, Xiaoshu Hamilton, Kindreth D McNicol, Ewan D and Zhu, Xiaoshu 2009. Cochrane Database of Systematic Reviews. Chuang, Pei-Chin Lin, Yiu-Juian Wu, Meng-Hsing Wing, Lih-Yuh C. Shoji, Yutaka and Tsai, Shaw-Jenq 2010. Inhibition of CD36-Dependent Phagocytosis by Prostaglandin E2 Contributes to the Development of Endometriosis. The American Journal of Pathology, Vol. 176, Issue. 2, p. 850. Lee, JeHoon Banu, Sakhila K. Rodriguez, Royce Starzinski-Powitz, Anna and Arosh, Joe A. 2010. Selective blockade of prostaglandin E2 receptors EP2 and EP4 signaling inhibits proliferation of human endometriotic epithelial cells and stromal cells through distinct cell cycle arrest. Fertility and Sterility, Vol. 93, Issue. 8, p. 2498. Larosa, M. Facchini, F. Pozzoli, G. Leone, M. Grande, M. and Monica, B. 2010. Endometriosis: Aetiopathogenetic Basis. Urologia Journal, Vol. 77, Issue. 17_suppl, p. 1. Machado, Daniel Escorsim Berardo, Plínio Tostes Landgraf, Richardt Gama Fernandes, Patrícia Dias Palmero, Celia Alves, Leandro Miranda Abrao, Maurício Simões and Nasciutti, Luiz Eurico 2010. A selective cyclooxygenase-2 inhibitor suppresses the growth of endometriosis with an antiangiogenic effect in a rat model. Fertility and Sterility, Vol. 93, Issue. 8, p. 2674. Azizabadi Farahani, M. and Assari, S. 2010. Handbook of Disease Burdens and Quality of Life Measures. p. 3933. Chen, Tsung-Ming Hsu, Chien-Hui Tsai, Shaw-Jenq and Sun, H. Sunny 2010. AUF1 p42 isoform selectively controls both steady-state and PGE2-induced FGF9 mRNA decay. Nucleic Acids Research, Vol. 38, Issue. 22, p. 8061.

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Condition tags

mesh:D004715endometriosischronic_pelvic_paindysmenorrheadyspareuniainfertility

MeSH descriptors

Endometriosis Endometriosis Prostaglandins Cell Proliferation Cell Proliferation Endometriosis Endometriosis Estrogens Estrogens Female Fibroblast Growth Factor 9 Fibroblast Growth Factor 9 Humans Prostaglandins Stromal Cells Stromal Cells Stromal Cells

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