Role of reactive oxygen species in the renal fibrosis
Role of reactive oxygen species in the renal fibrosis
复制标题
活性氧在肾纤维化中的作用
DOI：
10.3760/cma.j.issn.0366-6999.2012.14.035
复制
发表时间：
2012-07-20
影响因子：
6.1
通讯作者：
Hou Fan-fan
中科院分区：
文献类型：
--
作者：
Nie Jing;Hou Fan-fan
肾纤维化是导致终末期肾病的进行性肾病的常见途径，无论病因如何。越来越多的证据表明，氧化应激导致活性氧（ROS）的产生，在纤维化疾病的发生和发展中起着至关重要的作用。烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶是ROS产生的主要酶源，目前被认为是肾脏疾病中细胞增殖和基质蓄积的关键介质。多种刺激物和激动剂，如转化生长因子β 1、肿瘤坏死因子、血小板衍生生长因子、血管紧张素II、高血糖症、氧化低密度脂蛋白和白蛋白，已显示可改变NADPH氧化酶的活性或表达，并最终增加ROS的产生。活性氧直接引发生物学重要大分子的损伤，导致所谓晚期氧化蛋白产物（AOPP）和晚期糖基化终产物的产生，它们不仅是氧化应激的标志物，而且还会导致肾损伤。靶向NADPH氧化酶和/或减少AOPP的产生可能是各种纤维化肾脏疾病治疗干预的新策略。中华医学杂志2012;125（14）：2598-2602
Renal fibrosis is a common pathway of progressive renal diseases leading to end-stage renal disease regardless of the etiology. Accumulating evidence indicates that oxidative stress, resulting in generation of reactive oxygen species (ROS), plays a critical role in the initiation and progression of fibrotic diseases. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the predominant enzyme source for ROS generation and is now recognized as a key mediator of cell proliferation and matrix accumulation in renal disease. Multiple stimuli and agonists, such as transforming growth factor beta 1, tumor necrosis factor, platelet derived growth factor, angiotensin II, hyperglycemia, oxidized low-density lipoprotein and albumin have been shown to alter the activity or expression of the NADPH oxidase and ultimately increase ROS production. ROS directly incites damage to biologically important macromolecules and leads to generation of the so-called advanced oxidation protein products (AOPPs) and advanced glycation end products, which are not only markers of oxidative stress but also cause renal injury. Targeting NADPH oxidase and/or reducing AOPPs production might be a novel strategy for the therapeutic intervention of variety of fibrotic kidney disorders. Chin Med J 2012;125(14):2598-2602