Reactive Oxygen Species and Redox Signaling in Chronic Kidney Disease.
Maria V IrazabalVicente E TorresPublished in: Cells (2020)
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.
Keyphrases
- reactive oxygen species
- chronic kidney disease
- oxidative stress
- public health
- nuclear factor
- cell death
- end stage renal disease
- dna damage
- hydrogen peroxide
- anti inflammatory
- toll like receptor
- signaling pathway
- type diabetes
- risk factors
- drinking water
- coronary artery disease
- epithelial mesenchymal transition
- cell free
- cardiovascular events
- circulating tumor cells
- electron transfer