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NF-κB相关信号通路在肾缺血-再灌注损伤中作用的研究进展 被引量:5

Research progress of NF-κB signaling pathway in kidney ischemia-reperfusion injury
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摘要 肾缺血-再灌注损伤(IRI)是肾移植和肾部分切除术后预后不佳的主要原因,同时也是急性肾损伤的重要病理生理过程,因此,肾IRI的防治对于改善肾移植预后具有重要意义。然而,IRI的机制较为复杂,其具体机制尚未明确。炎症反应作为IRI主要发病机制之一,在IRI导致的肾损伤中具有重要意义。核因子(NF)-κB作为一种快速反应转录因子,被证实在肾IRI中参与炎症反应的调控。因此,本文将从NF-κB的结构组成、NF-κB信号通路的激活途径及肾IRI中NF-κB上游信号通路和下游信号通路的调控机制进行综述,探讨NF-κB相关信号通路在肾IRI中的作用,为肾IRI的防治提供新的临床思路。 Kidney ischemia-reperfusion injury(IRI)is the major cause of poor prognosis after kidney transplantation and partial nephrectomy.Besides,it is also a critical pathophysiological process of acute kidney injury.Consequently,the prevention and treatment of kidney IRI are of significance to improve clinical prognosis of recipients undergoing kidney transplantation.However,the mechanism underlying IRI is complex,and the exact mechanism remains elusive.Inflammation,as one of the main pathogenesis of IRI,plays a significant role in IRI-induced kidney injury.Nuclear factor(NF)-κB,as a rapid response transcription factor,has been proven to be involved in the regulation of inflammation during kidney IRI.Therefore,in this article,the structure of NF-κB,the activation pattern of NF-κB signaling pathway,the regulatory mechanisms of NF-κB upstream and downstream signaling pathways in kidney IRI were reviewed,and the role of NF-κB signaling pathway in kidney IRI was investigated,aiming to provide novel clinical ideas for the prevention and treatment of kidney IRI.
作者 张瑞波 申开文 袁强 王强 沈俊 Zhang Ruibo;Shen Kaiwen;Yuan Qiang;Wang Qiang;Shen Jun(Guizhou Medical University,Guiyang 550004,China;不详)
出处 《器官移植》 CAS CSCD 北大核心 2022年第3期349-355,共7页 Organ Transplantation
基金 贵州省卫生健康委科学技术基金(gzwkj2021-220) 贵州省科技计划项目[(2018)5779-6] 国家自然科学基金培育项目(贵州医科大学附属医院)[gyfynsfc(2020)-30]。
关键词 肾移植 核因子-κB 炎症反应 缺血-再灌注损伤 多聚腺苷二磷酸核糖聚合酶-1 TOLL样受体4 NOD样受体蛋白3 缺氧诱导因子-1Α Kidney transplantation Nuclear factor-κB Inflammation Ischemia-reperfusion injury Poly adenosine-diphosphate-ribose polymerase-1 Toll-like receptor 4 NOD-like receptor protein 3 Hypoxia inducible factor-1α
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