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.

IL15 promotes growth and invasion of endometrial stromal cells and inhibits killing activity of NK cells in endometriosis

“…Compared with normal endometria, a remarkable activation of the autophagic process was observed in ectopic endometrial lesions (Nasu et al 2011). It is also evident that transcriptional induction of autophagyrelated genes (i.e.…”

MicroRNA expression profiles and networks in CXCL12-stimulated human endometrial stromal cells

“…Endometriotic tissue exhibits various molecular differences compared with healthy endometrial tissue, including variations in gene expression, production of proteins, responsiveness to steroids and cytokines, immune components, adhesion molecules, and proteolytic enzymes (15,16). The occurrence and development of endometriosis may be based on these aberrations in molecular processes, and may be caused by as yet unknown triggers, including miRNA, which initiate these molecular alterations.…”

“…Certain studies have investigated the role of miRNA expression dysregulation, histone modification and DNA methylation in endometriotic cells (17). Aberrant gene expression associated with epigenetic mechanisms may induce differentiation and the subsequent appearance of an endometriotic phenotype in healthy endometrial cells (15,16). …”

Gene Polymorphisms in FAS (Rs3740286 and Rs4064) Are Involved in Endometriosis Development in Brazilian Women, but not those in CASP8 (rs13416436 and rs2037815)

“…[8][9][10] Another study reviewed the role of apoptosis-associated molecules in the treatment of endometriosis with potential clinical applications in the future. 11 Single nucleotide polymorphisms (SNPs) in apoptotic genes, such as those of the Fas cell surface death receptor (FAS) and the caspase-8 (CASP8) genes, may be involved with the development of endometriosis.…”