title: Aberrant expression of apoptosis-related molecules in endometriosis: a possible mechanism underlying the pathogenesis of endometriosis.
abstract: Endometriosis, a disease affecting 3% to 10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue under the influence of estrogen. It is also becoming recognized as a condition in which ectopic endometrial cells exhibit abnormal proliferative and apoptotic regulation in response to appropriate stimuli. Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggests that, in healthy women, endometrial cells expelled during menstruation do not survive in ectopic locations because of programmed cell death, while decreased apoptosis may lead to the ectopic survival and implantation of these cells, resulting in the development of endometriosis. Both the inability of endometrial cells to transmit a "death" signal and the ability of endometrial cells to avoid cell death have been associated with increased expression of antiapoptotic factors and decreased expression of preapoptotic factors. Further investigations may elucidate the role of apoptosis-associated molecules in the pathogenesis of endometriosis. Medical treatment with apoptosis-inducing agents may be novel and promising therapeutic strategy for endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Oita, Japan. nasu@oita-u.ac.jp
authors.forename: Kaei
authors.initials: K
authors.lastname: Nasu
authors.forename: Masakazu
authors.initials: M
authors.lastname: Nishida
authors.forename: Yukie
authors.initials: Y
authors.lastname: Kawano
authors.forename: Akitoshi
authors.initials: A
authors.lastname: Tsuno
authors.forename: Wakana
authors.initials: W
authors.lastname: Abe
authors.forename: Akitoshi
authors.initials: A
authors.lastname: Yuge
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Takai
authors.forename: Hisashi
authors.initials: H
authors.lastname: Narahara
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D004715:Endometriosis / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D004717:Endometrium / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation; D019254:Genes, bcl-2; D018816:Genes, cdc; D006801:Humans; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis / Q000235:genetics
chemical_list: D017346:Protein Serine-Threonine Kinases