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Role of NLRP3 inflammasome in the development of bladder pain syndrome interstitial cystitis

机译:NLRP3炎性小体在膀胱疼痛综合征间质性膀胱炎发展中的作用

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摘要

Although it has been proposed that NOD-like receptor protein 3 (NLRP3) inflammasome activation may have an important contribution to the onset of bladder pain syndrome/interstitial cystitis (BPS/IC), as of today there is still insufficient evidence to accept or to reject this hypothesis. However, taking into consideration that inflammasomes have been already shown as important mediators of cyclophosphamide-induced bladder inflammation and that some studies have also revealed human bladder epithelium expresses high levels of NLRP3, such a hypothesis seems to be reasonable. The purpose of this review is to discuss a scenario that NLRP3 inflammasome is a crucial player in the development of this disease. Identification of a novel mediator of bladder inflammation and pain could lead to emerging new therapeutic strategy and the first causative therapy.
机译:尽管有人提出NOD样受体蛋白3(NLRP3)炎性小体激活可能对膀胱疼痛综合征/间质性膀胱炎(BPS / IC)的发作有重要贡献,但迄今为止,仍然没有足够的证据接受或接受拒绝这个假设。但是,考虑到炎症小体已被证明是环磷酰胺诱导的膀胱炎症的重要介质,并且一些研究还显示人膀胱上皮表达高水平的NLRP3,这种假设似乎是合理的。本文的目的是讨论NLRP3炎性小体是该病发展的关键因素的情况。膀胱炎症和疼痛的新型介体的鉴定可能导致出现新的治疗策略和第一种病因疗法。

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