Endometrial cell apoptosis impairment associated with hormonal imbalance as a key factor in the development of endometriosis

The review describes the effect of certain hormones and their imbalance on apoptosis of retrogradely refluxed endometrial cells in the abdominal cavity and the effects of estrogen, progesterone, anti-Mullerian hormone, and gonadotropin-releasing hormone on the internal and external apoptotic pathways of various cell populations in endometriotic foci. The nuclear estrogen receptor β (ER-β) is shown to inhibit TNF receptors that trigger the external apoptotic pathway, but the effects of estrogens do not play a key role in the pathogenesis of endometriosis. The role of progesterone and changes in the receptor status towards prevalence of PR-A with a decreased response of endometrial tissue to progesterone and inhibition of apoptosis are described. We discuss the role of the anti-Müllerian hormone and gonadotropin-releasing hormone II (GnRH II) as activators of apoptosis in normal endometrial tissue and in endometriosis. Investigation of endocrine effects on apoptosis of parenchymal and stromal cells of endometriotic foci may provide a theoretical basis for searching for new therapeutic targets in this hormone-dependent pathology.