Chronic kidney disease (CKD) remains a worldwide public health problem associated with serious complications and increased mortality rates. Accumulating evidence indicates that elevated intracellular levels of reactive oxygen species (ROS) play a major role in the pathogenesis of CKD. Increased intracellular levels of ROS can lead to oxidation of lipids, DNA, and proteins, contributing to cellular damage. On the other hand, ROS are also important secondary messengers in cellular signaling. Consequently, normal kidney cell function relies on the “right” amount of ROS. Mitochondria and NADPH oxidases represent major sources of ROS in the kidney, but renal antioxidant systems, such as superoxide dismutase, catalase, or glutathione peroxidase counterbalance ROS-mediated injury. This review discusses the main sources of ROS and antioxidant systems in the kidney, and redox signaling pathways leading to inflammation and fibrosis, which result in abnormal kidney function and CKD progression. We further discuss the important role of the nuclear factor erythroid 2-related factor 2 (Nrf2) in regulating antioxidant responses, and other mechanisms of redox signaling.

中文翻译：

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慢性肾脏病中的活性氧和氧化还原信号。

慢性肾脏病 (CKD) 仍然是一个世界性的公共卫生问题，与严重的并发症和死亡率增加有关。越来越多的证据表明，细胞内活性氧 (ROS) 水平升高在 CKD 的发病机制中起着重要作用。细胞内 ROS 水平升高可导致脂质、DNA 和蛋白质氧化，从而导致细胞损伤。另一方面，ROS 也是细胞信号传导中重要的二级信使。因此，正常的肾细胞功能依赖于“正确”量的 ROS。线粒体和 NADPH 氧化酶是肾脏中 ROS 的主要来源，但肾脏抗氧化系统，如超氧化物歧化酶、过氧化氢酶或谷胱甘肽过氧化物酶，可以平衡 ROS 介导的损伤。本综述讨论了肾脏中 ROS 和抗氧化系统的主要来源，以及导致炎症和纤维化的氧化还原信号通路，从而导致肾功能异常和 CKD 进展。我们进一步讨论了核因子红细胞 2 相关因子 2 (Nrf2) 在调节抗氧化反应和其他氧化还原信号机制中的重要作用。