期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 25, 期 12, 页码 657-684出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2016.6664
关键词
reactive oxygen species; NADPH-oxidases; diabetic nephropathy; albuminuria
资金
- National Health and Medical Research Council of Australia
- JDRF Program/ Project Grant
Significance: Intrarenal oxidative stress plays a critical role in the initiation and progression of diabetic kidney disease (DKD). Enhanced oxidative stress results from overproduction of reactive oxygen species (ROS) in the context of concomitant, insufficient antioxidant pathways. Renal ROS production in diabetes is predominantly mediated by various NADPH oxidases (NOXs), but a defective antioxidant system as well as mitochondrial dysfunction may also contribute. Recent Advances: Effective agents targeting the source of ROS generation hold the promise to rescue the kidney from oxidative damage and prevent subsequent progression of DKD. Critical Issues and Future Directions: In the present review, we summarize and critically analyze molecular and cellular mechanisms that have been demonstrated to be involved in NOX-induced renal injury in diabetes, with particular focus on the role of increased glomerular injury, the development of albuminuria, and tubulointerstitial fibrosis, as well as mitochondrial dysfunction. Furthermore, novel agents targeting NOX isoforms are discussed.
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