摘要
背景:临床上治疗子宫内膜异位症仍具有挑战性。为了改善这种情况,我们在针对病因和病理过程的病理生理机制发展了新的治疗策略。 方法:不断更新的研究数据针对不同的治疗给出了进一步的总结。 结果:炎症复合物被认为是一种多重蛋白复合物并且被认为是调节细胞溶质和其他隔室进入细胞的先天和适应性宿主反应的关键调节剂。它参与DAMPs的危险分子模式和PAMPs致病分子模式存在的直接检测和应答,被认为存在于许多细胞中,主要是免疫细胞的骨髓谱系和上皮细胞组织粘膜表面。四种炎症复合物以不用组成的刺激组成方式形成,分别是NLR蛋白Nlrp1b、Nlrp3、Nlrc4、Nlrp6,同时不存在于黑色素瘤2中。他们激活诱导宿主反应的IL-β和IL-18的产生,例如焦虫病,促炎细胞死亡和无前导序列的细胞因子和生长因子的分泌。炎症复合物与动脉粥样硬化、定期发烧综合征、白癜风、克罗恩病、痛风和失眠沉淀证、硅肺病、阿尔兹海默症和牙周炎有关。子宫内膜异位症与IL-1β有关,另一种NLR,NIrp7与人子宫内膜癌组织中子宫肌层浸润相关。 结论:关于子宫内膜异位症治疗的未来发展,关于炎性细胞的致病机制的新线索是至关重要的。
关键词: 分子,通路,炎症,NLRP-3,DAMP
Current Drug Targets
Title:Inflammasome as a Key Pathogenic Mechanism in Endometriosis
Volume: 18 Issue: 9
关键词: 分子,通路,炎症,NLRP-3,DAMP
摘要: Background: Endometriosis remains a challenging condition for clinicians to treat. To improve our results, we have to develop new treatment strategies based on pathophysiological mechanisms targeting the etiologic and pathogenic processes involved.
Objectives: Revise new inflammatory pathogenic mechanisms involved in endometriosis, namely inflammasome. Method: Literature review for the updating of data to give new clues for different options of treatments. Results: Inflammasome has been described as a multiprotein complex and is considered a key regulator of the innate and adaptive host response that surveys the cytosol and other compartments into the cell. It is involved in the immediate detection and responds to the presence of danger- and pathogen-associated molecular patterns named DAMPs and PAMPs respectively, and has been described in several cells, mainly on immune cells of the myeloid lineage and epithelial cells in tissues with mucosal surfaces. Four inflammasome are formed in a stimulus-dependent manner of distinct composition. They are the Noll Like Receptors (NLR) proteins Nlrp1b, Nlrp3, Nlrc4, and Nlrp6, as well as the absent in melanoma 2 (AIM2). They activate the production of IL-1β and IL-18 that induce a host response such as pyroptosis, a proinflammatory cell death and the secretion of leaderless cytokines and growth factors. Inflammasome is linked to atherosclerosis, periodic fever syndromes, vitiligo, Crohn’s disease, gout, asbestosis, silicosis, Alzheimer’s disease and periodontitis. Endometriosis has been related with IL-1β and Another NLR, Nlrp7, was correlated with myometrial invasion in human endometrial cancer tissue. Conclusions: These new clues regarding the pathogenic mechanisms involving the inflammasome may be crucial in the future development for endometriosis therapy.Export Options
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Cite this article as:
Inflammasome as a Key Pathogenic Mechanism in Endometriosis, Current Drug Targets 2017; 18 (9) . https://dx.doi.org/10.2174/1389450117666160709013850
DOI https://dx.doi.org/10.2174/1389450117666160709013850 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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