Department of Medicine, University of Illinois at Chicago, Chicago, IL 60607, United States.
Curr Gene Ther. 2017;17(6):405-410. doi: 10.2174/1566523218666180214092219.
Acute kidney injury has been a tough complex with increased mortality and morbidity. Inflammatory responses, including innate and adaptive immune responses, involve in the initiation and development of acute kidney injury, especially under the ischemic circumstances. Tubular cells and distinct immune cell subgroups play a critical role in the pathogenesis of inflammation. Current gene therapies show their benefits in renal repair. Here, we reviewed the renal inflammatory infiltration, inflammatory mediators, oxidative stress and potential signaling pathways, which give rise to the kidney diseases, in the mechanism of acute kidney injury. Recent studies showed diverse insights in understanding the pathophysiological process of inflammation related renal injury and provided novel clinical targets for ameliorating acute kidney injury by balancing the facilitation of repairing and prevention of impairing. Interestingly, antisense oligonucleotides of target sequence, local electransfering on solid organ and adenovirus-mediated certain gene overexpression have been promising strategies in alleviating acute kidney injury.
急性肾损伤是一种死亡率和发病率增加的复杂疾病。炎症反应,包括先天和适应性免疫反应,参与急性肾损伤的发生和发展,特别是在缺血情况下。管状细胞和不同的免疫细胞亚群在炎症发病机制中起关键作用。目前的基因治疗在肾脏修复中显示出了它们的益处。在这里,我们综述了急性肾损伤发病机制中肾脏炎症浸润、炎症介质、氧化应激和潜在信号通路,这些因素导致了肾脏疾病。最近的研究表明,在理解与炎症相关的肾损伤的病理生理过程方面有了不同的见解,并通过平衡促进修复和预防损害的作用,为改善急性肾损伤提供了新的临床靶点。有趣的是,针对靶序列的反义寡核苷酸、固体器官的局部电转移和腺病毒介导的特定基因过表达已成为缓解急性肾损伤的有前途的策略。