Reactive Oxygen Species and Redox Signaling in Chronic Kidney Disease

Research output: Contribution to journalReview article

2 Scopus citations

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.

Original languageEnglish (US)
JournalCells
Volume9
Issue number6
DOIs
StatePublished - May 28 2020

Keywords

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

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