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Review
. 2016:2016:7813072.
doi: 10.1155/2016/7813072. Epub 2016 Aug 15.

Role of NADPH Oxidase in Metabolic Disease-Related Renal Injury: An Update

Cheng Wan  1 , Hua Su  1 , Chun Zhang  1
Affiliations
Review

Role of NADPH Oxidase in Metabolic Disease-Related Renal Injury: An Update

Cheng Wan et al. Oxid Med Cell Longev. 2016.

Abstract

Metabolic syndrome has been linked to an increased risk of chronic kidney disease. The underlying pathogenesis of metabolic disease-related renal injury remains obscure. Accumulating evidence has shown that NADPH oxidase is a major source of intrarenal oxidative stress and is upregulated by metabolic factors leading to overproduction of ROS in podocytes, endothelial cells, and mesangial cells in glomeruli, which is closely associated with the initiation and progression of glomerular diseases. This review focuses on the role of NADPH oxidase-induced oxidative stress in the pathogenesis of metabolic disease-related renal injury. Understanding of the mechanism may help find potential therapeutic strategies.

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Figures

Figure 1
Figure 1
NADPH oxidase-derived ROS in the pathogenesis of metabolic disease-related renal injury. Metabolic stimuli may upregulate the expression of NADPH oxidase and enhance the activity of NADPH oxidase, which subsequently leads to overproduction of ROS. NADPH oxidase-derived oxidative stress is involved in podocyte injury, endothelial dysfunction, mesangial proliferation, and so forth, eventually resulting in renal injury. NADPH: nicotinamide adenine dinucleotide phosphate; ROS: reactive oxygen species; NO: nitric oxide.
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