Bruner-Tran K L, Herington J L, Duleba A J, Taylor H S, Osteen K G
Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Minerva Ginecol. 2013 Apr;65(2):199-213.
Progesterone action normally mediates the balance between anti-inflammatory and proinflammatory processes throughout the female reproductive tract. However, in women with endometriosis, endometrial progesterone resistance, characterized by alterations in progesterone responsive gene and protein expression, is now considered a central element in disease pathophysiology. Recent studies additionally suggest that the peritoneal microenvironment of endometriosis patients exhibits altered physiological characteristics that may further promote inflammation-driven disease development and progression. Within this review, we summarize our current understanding of the pathogenesis of endometriosis with an emphasis on the role that inflammation plays in generating not only the progesterone-resistant eutopic endometrium but also a peritoneal microenvironment that may contribute significantly to disease establishment. Viewing endometriosis from the emerging perspective that a progesterone resistant endometrium and an immunologically compromised peritoneal microenvironment are biologically linked risk factors for disease development provides a novel mechanistic framework to identify new therapeutic targets for appropriate medical management.
孕酮作用通常介导整个女性生殖道抗炎和促炎过程之间的平衡。然而，在子宫内膜异位症患者中，以孕酮反应性基因和蛋白表达改变为特征的子宫内膜孕酮抵抗，现在被认为是疾病病理生理学的核心要素。最近的研究还表明，子宫内膜异位症患者的腹膜微环境表现出改变的生理特征，这可能进一步促进炎症驱动的疾病发展和进展。在这篇综述中，我们总结了目前对子宫内膜异位症发病机制的理解，重点强调炎症不仅在产生孕酮抵抗的在位内膜中起作用，而且在可能对疾病发生有重大贡献的腹膜微环境中也起作用。从新出现的观点来看，孕酮抵抗的内膜和免疫受损的腹膜微环境是疾病发展的生物学相关危险因素，这为识别适当医学管理的新治疗靶点提供了一个新的机制框架。
