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Mitochondrial integrity and function in atherogenesis.

Scott W Ballinger1, Cam Patterson, Cynthia A Knight-Lozano

  • 1Sealy Center for Molecular Cardiology and Division of Cardiology, The University of Texas Medical Branch, Galveston, Tex, USA.

Circulation
|July 31, 2002
PubMed
Summary
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Mitochondrial DNA damage, caused by reactive oxygen and nitrogen species, is an early event in the development of atherosclerosis. This damage contributes to vascular cell dysfunction and disease progression.

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Oxidative Stress

Background:

  • Coronary atherosclerotic disease is a leading cause of death.
  • Reactive oxygen and nitrogen species (RS) contribute to vascular cell dysfunction and atherogenesis.
  • Oxidative damage to mitochondrial DNA leads to mitochondrial dysfunction.

Purpose of the Study:

  • To investigate the role of mitochondrial oxidant generation and DNA damage in the progression of atherosclerotic lesions.
  • To examine the relationship between mitochondrial DNA damage and atherosclerosis in human and mouse models.

Main Methods:

  • Analysis of human arterial specimens.
  • Study of atherosclerosis-prone apolipoprotein E(-/-) mice.
  • Assessment of mitochondrial DNA damage and atherosclerotic lesion extent.

Related Experiment Videos

  • Evaluation of mice deficient in manganese superoxide dismutase.

    • Main Results:

    • Mitochondrial DNA damage correlated with atherosclerosis extent in human specimens and mouse aortas.
    • Mitochondrial DNA damage preceded atherogenesis in young apolipoprotein E(-/-) mice.
    • Mice lacking manganese superoxide dismutase showed increased mitochondrial DNA damage and accelerated atherogenesis.

    Conclusions:

    • Mitochondrial DNA damage, potentially from reactive oxygen and nitrogen species, may be an early event in atherosclerotic lesion initiation.
    • This damage contributes to vascular dysfunction and the progression of atherosclerosis.