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Impairing eukaryotic elongation factor 2 kinase activity decreases atherosclerotic plaque formation

Peng Zhang1, Maziar Riazy1, Matthew Gold2

  • 1Department of Medicine, University of British Columbia and Vancouver Coastal Health Research Institute, Vancouver, British Columbia, Canada.

The Canadian Journal of Cardiology
|December 6, 2014
PubMed

Insights

Loss of eukaryotic elongation factor 2 kinase (eEF2K) in macrophages significantly reduced atherosclerosis development in mice. Inhibiting eEF2K may offer a new therapeutic strategy for treating atherosclerosis.

Area of Science:

  • Cardiovascular biology
  • Immunology
  • Molecular biology

Background:

  • Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
  • Macrophage function plays a critical role in the development and progression of atherosclerotic lesions.
  • Eukaryotic elongation factor 2 kinase (eEF2K) is a key regulator of protein synthesis, but its role in atherosclerosis is not well understood.

Purpose of the Study:

  • To investigate the role of eEF2K activity in macrophages on the development of atherosclerosis.
  • To determine if inhibiting eEF2K can suppress atherosclerotic plaque formation.

Main Methods:

  • Bone marrow from mice with mutant eEF2K was transplanted into low-density lipoprotein receptor-deficient (ldlr(-/-)) mice.
  • Mice were fed a high-fat diet for 16 weeks to induce atherosclerosis.
  • Analysis of atherosclerotic plaque formation and macrophage inflammatory markers.

Main Results:

  • Mice receiving mutant eEF2K bone marrow (hematopoietic chimeras) exhibited significantly reduced atherosclerotic plaque formation compared to controls.
  • M1-skewed macrophages from eEF2K knock-in mice showed decreased tumor necrosis factor-alpha release.
  • These macrophages also demonstrated a reduced ability to induce endothelial cell marker expression.

Conclusions:

  • eEF2K activity in hematopoietic cells contributes to the development of atherosclerosis.
  • Targeting eEF2K may represent a novel therapeutic approach for managing atherosclerosis.
  • Further research into eEF2K inhibitors for atherosclerosis treatment is warranted.

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