Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Biomed Res Int. 2013;2013:839761. doi: 10.1155/2013/839761. Epub 2013 Nov 11.
Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.
蛋白尿是终末期肾病（ESRD）的一个独立危险因素（Shankland，2006）。最近的研究强调了足细胞损伤的机制及其在蛋白尿性肾脏疾病中潜在治疗策略的意义（Zhang 等人，2012）。活性氧（ROS）是与肾小球硬化的发生和进展密切相关的细胞信号。NADPH 氧化酶是细胞 ROS 产生的一个有区别的酶源，在足细胞中明显表达（Zhang 等人，2010）。在过去的十年中，已经明显的是，NADPH 氧化酶衍生的 ROS 过度产生是足细胞损伤的一个关键触发因素，如肾素-血管紧张素-醛固酮系统的激活（Whaley-Connell 等人，2006）、上皮-间充质转化（Zhang 等人，2011）和炎症启动（Abais 等人，2013）。这篇综述重点讨论了在不同病理生理条件下 NADPH 氧化酶介导的 ROS 对足细胞损伤的作用机制。此外，我们还回顾了 NADPH 氧化酶在与足细胞损伤相关的肾脏疾病中的治疗前景。
