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Updated: Mar 15, 2026

Bioluminescence Imaging of NADPH Oxidase Activity in Different Animal Models
Published on: October 22, 2012
Role of NADPH Oxidase in Metabolic Disease-Related Renal Injury: An Update
Cheng Wan1, Hua Su1, Chun Zhang1
1Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.
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.
Insights
Metabolic syndrome increases chronic kidney disease risk. NADPH oxidase-induced oxidative stress in kidney cells drives this injury, offering potential therapeutic targets.
Area of Science:
- Nephrology
- Metabolic Diseases
- Oxidative Stress
Background:
- Metabolic syndrome is a known risk factor for chronic kidney disease (CKD).
- The precise mechanisms linking metabolic dysfunction to kidney damage are not fully understood.
- Oxidative stress is implicated in the progression of kidney diseases.
Purpose of the Study:
- To review the role of NADPH oxidase in metabolic syndrome-related kidney injury.
- To elucidate the contribution of oxidative stress to glomerular diseases in metabolic syndrome.
- To identify potential therapeutic avenues targeting NADPH oxidase.
Main Methods:
- Literature review focusing on NADPH oxidase and kidney disease.
- Analysis of studies investigating oxidative stress in podocytes, endothelial cells, and mesangial cells.
- Synthesis of evidence linking metabolic factors to reactive oxygen species (ROS) production.
Main Results:
- NADPH oxidase is a primary source of intrarenal oxidative stress.
- Metabolic factors upregulate NADPH oxidase activity.
- Overproduction of ROS by NADPH oxidase contributes to glomerular cell damage and disease initiation/progression.
Conclusions:
- NADPH oxidase-driven oxidative stress is a key player in metabolic syndrome-related renal injury.
- Understanding this pathway is crucial for developing targeted therapies for CKD in metabolic syndrome patients.
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