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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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NOX enzymes and diabetic complications

Tomoko Kakehi1, Chihiro Yabe-Nishimura

  • 1Department of Pharmacology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyoku, Kyoto, Japan.

Seminars in Immunopathology
|May 20, 2008
PubMed

Insights

High blood sugar damages tissues through several pathways, including increased reactive oxygen species (ROS). Suppressing NADPH oxidase, which generates ROS downstream of key pathways, may treat diabetic complications.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Hyperglycemia triggers multiple molecular mechanisms leading to tissue damage.
  • Key pathways include the polyol and hexosamine pathways, advanced glycation end product formation, protein kinase C activation, and reactive oxygen species (ROS) generation.

Purpose of the Study:

  • To elucidate the role of NADPH oxidase in hyperglycemia-induced tissue damage.
  • To identify NADPH oxidase as a potential therapeutic target for diabetic complications.

Main Methods:

  • Review of experimental data on molecular mechanisms of hyperglycemia.
  • Analysis of the signaling cascade involving ROS and NADPH oxidase.

Main Results:

  • Increased ROS production contributes to cellular damage and activates specific gene expression.
  • NADPH oxidase activity is upregulated downstream of advanced glycation end products and protein kinase C pathways in hyperglycemia-vulnerable tissues.

Conclusions:

  • NADPH oxidase plays a significant role in the pathogenesis of diabetic complications.
  • Inhibiting NADPH oxidase activity presents a promising therapeutic strategy for ameliorating diabetic complications.

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