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NOX, NOX Who is There? The Contribution of NADPH Oxidase One to Beta Cell Dysfunction

David A Taylor-Fishwick1

  • 1Department of Internal Medicine, Strelitz Diabetes Center, Eastern Virginia Medical School Norfolk, VA, USA ; Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School Norfolk, VA, USA.

Frontiers in Endocrinology
|April 9, 2013
PubMed

Insights

Reactive oxygen species (ROS) contribute to diabetes by damaging beta cells. Targeting NADPH oxidase-1 (NOX-1) and its signaling pathways offers a new strategy to protect beta cell mass.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • Diabetes prevalence necessitates novel strategies to preserve pancreatic beta cell mass.
  • Beta cells are vulnerable to oxidative stress, leading to dysfunction.
  • NADPH oxidases (NOX) are identified as key contributors to elevated reactive oxygen species (ROS) in beta cells.

Purpose of the Study:

  • To review recent findings on the role of NADPH oxidase-1 (NOX-1) in beta cell dysfunction.
  • To integrate pathways regulating NOX-1 in the context of diabetes-associated inflammation.
  • To identify NOX-1 as a potential therapeutic target for preserving beta cell function.

Main Methods:

  • Literature review of recent reports on NOX-1 and beta cell dysfunction.
  • Analysis of cytokine-stimulated NOX-1 expression regulation by inflammatory lipid mediators.
  • Examination of NOX-1 regulation via ROS and Src-kinase activation in beta cells.

Main Results:

  • Cytokine-stimulated NOX-1 expression is linked to 12-lipoxygenase-derived lipid mediators, integrating distinct dysfunction pathways.
  • NOX-1 regulation involves feed-forward control with ROS and Src-kinase, potentially causing excessive ROS generation.
  • Selective NOX-1 inhibitors are emerging as potential therapeutic agents.

Conclusions:

  • NOX-1 plays a significant role in diabetes-related beta cell dysfunction.
  • The NOX-1/ROS signaling pathway presents a novel target for pharmacologic intervention.
  • Disrupting NOX-1 signaling may offer a new approach to protect beta cell mass in diabetes.
Keywords:
NADPH oxidasebeta cell dysfunctioncytokinesreactive oxygen speciessrc-kinase

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