title: Future directions in endometriosis research.
abstract: Endometriosis is an estrogen-dependent condition that affects 5 million American women; however, its etiology is not fully understood. The development of the baboon model of endometriosis provides an extremely powerful tool to investigate the development and progression of endometriosis from the early invasive phase to the advanced established disease. The inflammatory reaction that occurs in the peritoneal cavity at the site of endometriotic lesions does not clear the refluxed endometrial fragments. Moreover, this reaction appears to promote the survival of the tissue and the development of the disease. Exploration of the interactions between peritoneal macrophages and cytotoxic T cells and endometrial cells will determine whether their ability to scavenge and induce apoptosis is altered. Determining the mechanism(s) that induces the expression of estrogen and its receptor (ERbeta) is crucial to our understanding of the progression of the disease. The effects of ERbeta activation in endometriotic lesions should be investigated. It is important to determine the effects of estrogen on the function of the immune cells, either directly or indirectly. Finally, determining the effect of events at sites of ectopic endometrium on the eutopic endometrium may elucidate the mechanism(s) of infertility associated with endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, College of Medicine, University of Illinois at Chicago, 820 South Wood Street, Chicago, IL 60612, USA.
authors.forename: Julie M
authors.initials: JM
authors.lastname: Hastings
authors.forename: Asgerally T
authors.initials: AT
authors.lastname: Fazleabas
mesh_terms: D004195:Disease Models, Animal; D018450:Disease Progression; D004715:Endometriosis / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006176:Gynecology / Q000379:methods / Q000639:trends*; D006728:Hormones / Q000378:metabolism; D006801:Humans; D011956:Receptors, Cell Surface / Q000378:metabolism; D012106:Research / Q000639:trends; D013256:Steroids / Q000378:metabolism; D014599:Uterus / Q000503:physiopathology
chemical_list: D006728:Hormones; D011956:Receptors, Cell Surface; D013256:Steroids