Reactive Oxygen Species and Redox Signaling in Chronic Kidney Disease

Cells

VicenteE. Torres¹  MariaV. Irazabal¹ 

[1] Department of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street, Rochester, MN 55905, USA;

关键词: chronic kidney disease;    reactive oxygen species;    oxidative stress;    mitochondria;    NADPH oxidases;    nuclear factor erythroid 2–related factor 2 (Nrf2);   

DOI  :  10.3390/cells9061342

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown