The Role of Apoptotic Dysfunction in the Pathogenesis of Endometriosis

Author(s): Kaei Nasu, Masakazu Nishida, Akitoshi Yuge, Noriyuki Takai, Hisashi Narahara

Journal Name: Current Women`s Health Reviews

Volume 3 , Issue 2 , 2007

Become EABM
Become Reviewer
Call for Editor


Endometriosis, a disease affecting 3-10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Increasingly, endometriosis 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 anti-apoptotic factors and decreased expression of pre-apoptotic factors. This paper is a review of the recent literature focused on the differential expression of apoptosis-associated molecules in the normal endometria of women without endometriosis, and in the eutopic and ectopic endometria of women with endometriosis. The role of apoptosis in the pathogenesis of endometriosis and the basic and clinical research on the treatment of endometriosis with apoptosis-inducing agents will be discussed.

Keywords: Endometriosis, apoptosis, proliferation, pathogenesis, medical treatment

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2007
Page: [113 - 122]
Pages: 10
DOI: 10.2174/1573404810703020113
Price: $65

Article Metrics

PDF: 3