Prostaglandin E 2 : the master of endometriosis?

Wu MH, Meng-Hsing Wu, Meng‐Hsing Wu, Chun-Wun Lu, Lu CW, Pei-Chin Chuang, Chuang PC, Pei‐Chin Chuang, Shaw‐Jenq Tsai, Shaw-Jenq Tsai
Experimental biology and medicine (Maywood, N.J.) · 2010 · vol. 235(6) , pp. 668–677 · doi:10.1258/ebm.2010.009321 · PMID:20511671 · W2024411072
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This review discusses recent advances in cellular and molecular mechanisms by which prostaglandin E2 contributes to the development of endometriosis, a condition associated with infertility and pain.

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Abstract

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.

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Condition tags

endometriosischronic_pelvic_paindysmenorrheadyspareuniainfertility

MeSH descriptors

Dinoprostone Endometriosis Endometriosis Dinoprostone Endometriosis Female Humans

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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Cited by (50)

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