Nitric oxide, oxidative stress, and p66Shc interplay in diabetic endothelial dysfunction

Biomed Res Int. 2014:2014:193095. doi: 10.1155/2014/193095. Epub 2014 Mar 5.

Abstract

Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production, p66Shc protein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging
  • Animals
  • Diabetes Mellitus / metabolism*
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / physiopathology*
  • Epigenesis, Genetic
  • Humans
  • Hydrogen Peroxide
  • Hypercholesterolemia / metabolism
  • Insulin / metabolism
  • Insulin Resistance
  • Mice
  • MicroRNAs / metabolism
  • Nitric Oxide / chemistry*
  • Nitric Oxide Synthase Type III / metabolism
  • Oxidative Stress*
  • Reactive Oxygen Species
  • Shc Signaling Adaptor Proteins / metabolism*
  • Signal Transduction
  • Src Homology 2 Domain-Containing, Transforming Protein 1
  • Vascular Diseases / physiopathology*

Substances

  • Insulin
  • MicroRNAs
  • Reactive Oxygen Species
  • SHC1 protein, human
  • Shc Signaling Adaptor Proteins
  • Src Homology 2 Domain-Containing, Transforming Protein 1
  • Nitric Oxide
  • Hydrogen Peroxide
  • Nitric Oxide Synthase Type III