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Oxidative stress and vein graft failure: a focus on NADH oxidase, nitric oxide and eicosanoids

Helen Weaver1, Nilima Shukla, David Ellinsworth

  • 1Bristol Heart Institute, University of Bristol, UK.

Current Opinion in Pharmacology
|April 17, 2012
PubMed

Insights

Superoxide and NADPH oxidase upregulation contribute to vein graft failure by promoting vascular smooth muscle cell proliferation and migration. Inhibiting NADPH oxidase may offer therapeutic strategies for preventing graft thickening.

Area of Science:

  • Cardiovascular Science
  • Vascular Biology
  • Biochemistry

Background:

  • Vein graft failure is a significant clinical challenge.
  • Superoxide and NADPH oxidase upregulation are implicated in graft failure pathogenesis.
  • Mechanisms include endothelial denudation, inflammatory cell factors, hypoxia, and altered eicosanoid signaling.

Purpose of the Study:

  • To review the role of NADPH oxidase in vein graft failure.
  • To discuss the impact of NADPH oxidase on neointima formation and metalloproteinase expression.
  • To explore therapeutic strategies targeting NADPH oxidase.

Main Methods:

  • Literature review focusing on NADPH oxidase in vein graft failure.
  • Analysis of mechanisms leading to NADPH oxidase upregulation.
  • Examination of downstream effects on vascular smooth muscle cells and matrix metalloproteinases.

Main Results:

  • NADPH oxidase upregulation is triggered by multiple factors post-implantation.
  • This leads to vascular smooth muscle cell replication and migration, contributing to neointima formation.
  • Enhanced metalloproteinase expression further drives graft thickening.

Conclusions:

  • NADPH oxidase plays a critical role in the development of vein graft failure.
  • Nitric oxide and eicosanoids are key mediators influenced by NADPH oxidase.
  • Inhibitors of NADPH oxidase activity and expression represent potential therapeutic targets.

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