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 E2 (PGE2), 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 PGE2 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.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)