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Related Experiment Videos

Oxidized low-density lipoprotein-induced apoptosis.

Robert Salvayre1, Nathalie Auge, Herve Benoist

  • 1INSERM U-466, Faculty of Medicine, University Paul Sabatier, CHU Rangueil, Avenue Jean Poulhès, 31054 Toulouse cedex 04, France. salvayre@toulouse.inserm.fr

Biochimica Et Biophysica Acta
|January 18, 2003
PubMed
Summary

Oxidized low-density lipoproteins (oxLDL) generate toxic compounds that trigger cell death pathways like apoptosis and necrosis. Understanding these mechanisms is crucial for studying atherosclerosis progression and potential treatments.

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Area of Science:

  • Cardiovascular Biology
  • Cellular Toxicology
  • Atherosclerosis Research

Background:

  • Low-density lipoproteins (LDL) become oxidized (oxLDL) within atherosclerotic lesions.
  • Oxidized LDL (oxLDL) possesses biological properties contributing to atherogenesis.
  • This review examines oxLDL toxicity and cell death mechanisms.

Purpose of the Study:

  • To review the toxic compounds generated during LDL oxidation.
  • To elucidate the features and mechanisms of oxLDL-induced apoptosis and necrosis.
  • To discuss the potential role of oxLDL-induced cell death in atherosclerosis.

Main Methods:

  • Review of literature on oxLDL toxicity and cellular responses.
  • Analysis of molecular pathways involved in oxLDL-induced cell death.

Related Experiment Videos

  • Examination of signaling pathways, oxidative stress, and calcium signaling.

    • Main Results:

    • Internalized oxLDL generates toxic lipid peroxides, oxysterols, and aldehydes.
    • These compounds induce oxidative stress, protein modification, and alter signaling.
    • OxLDL triggers a sustained calcium peak, leading to apoptosis or necrosis.
    • OxLDL-induced apoptosis involves mitochondrial and death-receptor pathways.
    • Necrosis occurs via a calcium-dependent pathway when apoptosis is inhibited.

    Conclusions:

    • Oxidized LDL (oxLDL) induces cell death through apoptosis and necrosis.
    • OxLDL-induced apoptosis and necrosis involve complex signaling and calcium pathways.
    • Apoptosis in atherosclerotic areas may contribute to plaque instability.
    • Further in vivo studies are needed to clarify the role of oxLDL in plaque cell death.