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[子宫内膜异位症:病因学与发病机制的新探讨(综述)]

[ENDOMETRIOSIS: A NEW APPROACH TO ETIOLOGY AND PATHOGENESIS (REVIEW)].

作者信息

Solopova A, Makacarya A, Chukanova E

机构信息

Federal State Autonomous Educational Institution of Higher Education I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation.

出版信息

Georgian Med News. 2017 Dec(273):7-11.

Abstract

Endometriosis is a dyshormonal immune-dependent genetically determined disease, which appears as an endometrioid tissue that grows outside the uterine. Endometriosis is one of the most urgent problems of medicine. To date, new concepts of the endometriosis etiology and pathogenesis have been developed, but, despite their abundance, there is no unified theory. Genetic and epigenetic factors result in changes in an expression of aromatase, steroidogenic factor 1, and estrogen receptors are suggested to be the main cause of endometriosis. These changes lead to an active synthesis of various pro-inflammatory agents and a nerve growth factor, that are important in the development of pain syndrome. Also, changes in the progesterone receptor functioning and the local progesterone resistance development decrease the antiproliferative activity, apoptosis, and the anti-inflammatory substances level, as well as increase the prostaglandin, metalloproteinase activity, and level of hypoxia factors. In addition, there are shreds of evidence that endometriosis is associated with the risk of malignant tumors development, so new concepts for understanding these mechanisms are actively developing. Some of these mechanisms are discussed in this review.

摘要

子宫内膜异位症是一种激素失调、免疫依赖且由基因决定的疾病,表现为生长在子宫外的子宫内膜样组织。子宫内膜异位症是医学上最亟待解决的问题之一。迄今为止,已经形成了关于子宫内膜异位症病因和发病机制的新观念,然而,尽管这些观念众多,但尚无统一的理论。遗传和表观遗传因素导致芳香化酶、类固醇生成因子1和雌激素受体的表达发生变化,这些被认为是子宫内膜异位症的主要病因。这些变化导致多种促炎因子和神经生长因子的活跃合成,而这些因子在疼痛综合征的发展中起重要作用。此外,孕酮受体功能的变化和局部孕酮抵抗的发展降低了抗增殖活性、细胞凋亡以及抗炎物质水平,同时增加了前列腺素、金属蛋白酶活性和缺氧因子水平。此外,有证据表明子宫内膜异位症与恶性肿瘤发生风险相关,因此,目前正在积极探索理解这些机制的新观念。本综述将讨论其中的一些机制。

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