Diabetes and kidney disease: Role of oxidative stress

Jay C. Jha, Claudine Banal, Bryna S M Chow, Mark E. Cooper, Karin Jandeleit-Dahm

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

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. Antioxid. Redox Signal. 25, 657-684.

Original languageEnglish
Pages (from-to)657-684
Number of pages28
JournalAntioxidants and Redox Signaling
Volume25
Issue number12
DOIs
Publication statusPublished - 20 Oct 2016

Keywords

  • albuminuria
  • diabetic nephropathy
  • NADPH-oxidases
  • reactive oxygen species

Cite this

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title = "Diabetes and kidney disease: Role of oxidative stress",
abstract = "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. Antioxid. Redox Signal. 25, 657-684.",
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Diabetes and kidney disease : Role of oxidative stress. / Jha, Jay C.; Banal, Claudine; Chow, Bryna S M; Cooper, Mark E.; Jandeleit-Dahm, Karin.

In: Antioxidants and Redox Signaling, Vol. 25, No. 12, 20.10.2016, p. 657-684.

Research output: Contribution to journalReview ArticleResearchpeer-review

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T1 - Diabetes and kidney disease

T2 - Role of oxidative stress

AU - Jha, Jay C.

AU - Banal, Claudine

AU - Chow, Bryna S M

AU - Cooper, Mark E.

AU - Jandeleit-Dahm, Karin

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AB - 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. Antioxid. Redox Signal. 25, 657-684.

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