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Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling

Shaw-Fang Yet1, Matthew D Layne, Xiaoli Liu

  • 1Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. syet@rics.bwh.harvard.edu.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|September 6, 2003
PubMed

Insights

Heme oxygenase-1 (HO-1) deficiency accelerates atherosclerosis and vein graft stenosis in mice. Loss of HO-1 increases vascular smooth muscle cell death, highlighting its protective role in vascular disease.

Area of Science:

  • Cardiovascular Biology
  • Vascular Pathophysiology
  • Enzymology

Background:

  • Heme oxygenase-1 (HO-1) is an enzyme involved in cellular protection.
  • Vascular diseases like atherosclerosis and vein graft stenosis pose significant health challenges.
  • The specific role of HO-1 in these vascular pathologies requires further elucidation.

Purpose of the Study:

  • To investigate the role of heme oxygenase-1 (HO-1) in the pathophysiology of atherosclerosis.
  • To determine the impact of HO-1 deficiency on vein graft stenosis.
  • To assess the protective mechanisms of HO-1 in vascular disease models.

Main Methods:

  • Generation of HO-1 deficient apolipoprotein E knockout mice (HO-1-/-apoE-/-).
  • Analysis of atherosclerotic lesion formation and composition in hypercholesterolemic mice.
  • Evaluation of neointimal formation and vascular smooth muscle cell (VSMC) death in a mouse vein graft stenosis model.

Main Results:

  • HO-1 deficient mice exhibited accelerated and more advanced atherosclerotic lesion formation compared to controls.
  • Vein grafts in HO-1 deficient mice showed increased neointima formation, followed by substantial VSMC death.
  • HO-1 deficient VSMC were more susceptible to oxidant stress-induced cell death.

Conclusions:

  • Heme oxygenase-1 (HO-1) plays a critical protective role in preventing atherosclerosis.
  • HO-1 deficiency exacerbates vein graft stenosis, primarily through increased VSMC death.
  • HO-1 is essential for vascular health and protection against oxidative stress in vascular diseases.

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