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Lack of the antioxidant enzyme glutathione peroxidase-1 accelerates atherosclerosis in diabetic apolipoprotein E-deficient mice.

Paul Lewis1, Nada Stefanovic, Josefa Pete

  • 1Oxidative Stress Group, JDRF Diabetes and Metabolism Division, Baker Heart Research Institute, PO Box 6492, St Kilda Rd Central, Melbourne, VIC 8008, Australia.

Circulation
|April 11, 2007

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View abstract on PubMed

Summary

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  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Lack Of The Antioxidant Enzyme Glutathione Peroxidase-1 Accelerates Atherosclerosis In Diabetic Apolipoprotein E-deficient Mice.
    • This summary is machine-generated.

    Glutathione peroxidase-1 (GPx1) deficiency accelerates atherosclerosis in diabetic mice by increasing inflammation and fibrosis. This highlights GPx1's protective role against diabetic macrovascular complications.

    Area of Science:

    • Cardiovascular Research
    • Metabolic Diseases
    • Antioxidant Biology

    Background:

    • Clinical studies suggest glutathione peroxidase-1 (GPx1) protects against diabetes-associated atherosclerosis.
    • The direct role of GPx1 in this process remains to be fully elucidated.

    Purpose of the Study:

    • To investigate the direct effect of GPx1 deficiency on diabetes-associated atherosclerosis.
    • To determine the impact of GPx1 on atherogenic pathways in a diabetic mouse model.

    Main Methods:

    • Diabetes was induced in apolipoprotein E-deficient (ApoE-/-) and GPx1/ApoE double-knockout (ApoE-/- GPx1-/-) mice.
    • Aortic lesion formation and atherogenic markers were assessed at 10 and 20 weeks.
    • Proinflammatory and profibrotic markers were quantified using RT-PCR and immunohistochemistry.

    Main Results:

    • Diabetic ApoE-/- GPx1-/- mice exhibited significantly increased atherosclerotic lesions compared to diabetic ApoE-/- mice.
    • Upregulation of macrophages, alpha-smooth muscle actin, RAGE, VCAM-1, VEGF, and CTGF was observed.
    • Increased nitrotyrosine levels indicated heightened oxidative stress in GPx1-deficient aortas.

    Conclusions:

    • GPx1 deficiency accelerates diabetes-associated atherosclerosis by promoting proinflammatory and profibrotic pathways.
    • GPx1 plays a crucial protective role in preventing diabetic macrovascular disease.
    • GPx1 emerges as a potential therapeutic target for diabetic macrovascular complications.

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