Abstract
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.
Highlights
Chronic kidney diseases (CKD) have multiple causes, which share the common feature of repetitive cycles of injury to the glomerular or tubular epithelium, associated with changes in cellular proliferation and repair, as well as activation of inflammatory processes, fibroblasts, and fibrosis, thereby resulting in nephron loss, decline in renal function and end-stage kidney disease (ESKD)
This review discusses the main sources of reactive oxygen species (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
This review focuses on 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
Summary
Chronic kidney diseases (CKD) have multiple causes, which share the common feature of repetitive cycles of injury to the glomerular or tubular epithelium, associated with changes in cellular proliferation and repair, as well as activation of inflammatory processes, fibroblasts, and fibrosis, thereby resulting in nephron loss, decline in renal function and end-stage kidney disease (ESKD). 22 of of 17 accumulation of ROS leads to inflammation, damage, and cell death, low levels of ROS are are required pro-survival signaling, proliferation,growth, growth,and andenergy energymetabolism metabolism [4,5,6]. Generated by several oxidase enzymes and the mitochondrial electron transport chain (ETC) It is Within the cells, is rapidly converted by superoxide dismutases 1 and 2 (SOD1 and 2) into the highly reactive and across primarily being transported through nonradical species. Have the capacity to modify redox-sensitive proteins accumulation of O2 is more commonly associated with oxidative stress, whereas H2 O2 is associated through thesignaling reversible of reactive cysteine residues, thereby regulate with redox [9].thiol
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