Journal
EXPERIMENTAL BIOLOGY AND MEDICINE
Volume 235, Issue 6, Pages 668-677Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1258/ebm.2010.009321
Keywords
angiogenesis; endometriosis; macrophage; phagocytosis; proliferation; prostaglandin; steroidogenesis; stromal cells
Categories
Funding
- National Science Council of Taiwan, Republic of China [NSC95-2320-B-006-047-MY3, 97-2314-B-006-020-MY3]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available