In a new study entitled “Estrogen Receptor β Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis,” as published in Cell, researchers have linked estrogen receptor β function to the pathogenesis of endometriosis and maintenance of an abnormal growth of endometrial tissue.
Study author Dr. Bert O’Malley, chair of molecular and cellular biology at Baylor College of Medicine, and colleagues had previously shed light on the molecular pathways underlying the inflammatory process in endometriosis, identifying a form of the steroid receptor coactivator -1 and its role in the promotion of endometriosis pathogenesis. Although endometriosis is considered an estrogen-driven disease, its molecular pathways are still unclear to the medical and research community. In this report, the team theorizes that a new protein network driven by estrogen receptor β (ER β) is involved in the onset and maintenance of endometriosis.
Researchers identified higher levels of the estrogen receptor β and enhanced ER β activity in human endometriotic tissues that further stimulated abnormal growth of uterine tissue outside of the uterus. Moreover, in mouse tissue, an inhibitory compound of ER β activity led to the suppression of endometriotic lesions’ growth. Importantly, gain of ERβ function led to endometriosis progression and increased the invasion activity of these harmful tissues.
Importantly, Professor O’Malley’s team revealed the mechanism behind ER β activity, whereby the receptor interacts with a cellular apoptotic pathway affecting the programmed cellular death induced by TNF –α. As a consequence, cells in the endometrial tissue escape the immune system surveillance system and continue to abnormally proliferate and induce further lesions.
In a press release, Dr. O’Malley said of the discovery: “This is an age-old problem that affects many women. As we unravel its molecular underpinnings, we come closer to finding an effective treatment.”
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