摘要
急性肾损伤(AKI)是一种常见的临床疾病,涉及多学科。由多种病因导致,整体发病率及死亡率较高。肾缺血再灌注损伤(IRI)作为AKI的主要发病机制之一,且炎症被认为是肾IRI发生发展中最重要的病理生理机制之一。单核细胞趋化蛋白1(MCP-1)已被证明与AKI有关。IκBα的磷酸化以及核转录因子-κB(NF-κB)信号通路的激活,可以释放MCP-1,并介导AKI的发生。相关的研究表明,IκBα主要通过泛素-蛋白酶体途径降解。本文通过阐述蛋白酶体抑制剂可通过抑制IκBα的磷酸化以及NF-κB信号通路的激活,从而阻止炎性因子的释放,以此来减轻AKI的机制,为蛋白酶体抑制剂治疗AKI的可能性提供前景。
Acute kidney injury(AKI) is a common clinical disease involving multiple disciplines. AKI is caused by a variety of causes, with a higher overall morbidity and mortality. Renal ischemia reperfusion injury(IRI) is one of the main pathogenesis of AKI, and inflammation is considered to be one of the most important pathophysiological mechanisms in the development of renal IRI. Monocyte chemoattractant protein 1(MCP-1) has been shown to be involved in AKI. Phosphorylation of IκBα and activation of the NF-κB signaling pathway release MCP-1 and mediate AKI. Related studies have shown that IκBα is mainly degraded by the ubiquitin-proteasome pathway. In this paper, proteasome inhibitors can inhibit the release of inflammatory factors by inhibiting the phosphorylation of IκBα and the activation of NF-κB signaling pathway, thereby alleviating the mechanism of AKI and providing prospects of possibility of treating AKI with proteasome inhibitors.
作者
韩博
于时良
王锐
安瑞华(审校)
HAN Bo;YU Shiliang;WANG Rui;AN Ruihua(Department of Urology,First Affiliated Hospital of Harbin Medical University,Harbin,150001,China)
出处
《临床泌尿外科杂志》
2020年第1期74-77,82,共5页
Journal of Clinical Urology
