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Pathogenesis of atherosclerosis

M Navab1, A M Fogelman, J A Berliner

  • 1Department of Medicine, University of California, Los Angeles, USA.

The American Journal of Cardiology
|September 28, 1995
PubMed
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Atherosclerosis begins with fatty streaks, driven by oxidized low-density lipoprotein (LDL) triggering inflammation and macrophage formation. High-density lipoprotein (HDL) may protect against these events.

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Lipid Metabolism

Background:

  • Atherosclerotic plaque development originates with fatty streaks.
  • This process involves low-density lipoprotein (LDL) trapping and oxidation within the artery wall.
  • Oxidized LDL triggers inflammatory responses, including monocyte recruitment and differentiation into macrophages.

Purpose of the Study:

  • To elucidate the early molecular events in atherosclerotic plaque formation.
  • To understand the role of oxidized LDL in initiating chronic inflammation.
  • To explore the potential protective mechanisms of high-density lipoprotein (HDL) against atherosclerosis.

Main Methods:

  • Analysis of the sequence of events in fatty streak development.
  • Investigation of LDL trapping, oxidation, and subsequent inflammatory signaling pathways (e.g., NF-κB).

Related Experiment Videos

  • Examination of the relationship between high-density lipoprotein (HDL) and the biological response to oxidized lipids.

    • Main Results:

    • Trapped LDL undergoes oxidation, initiating a cascade of inflammatory gene expression.
    • Activated transcription factors (NF-κB-like) mediate monocyte adhesion, chemotaxis, and macrophage conversion.
    • A specific gene influences LDL lipid oxidation and the biological response.
    • High-density lipoprotein (HDL) may counteract atherogenesis through lipid-modifying enzymes.

    Conclusions:

    • Fatty streak formation is an inflammatory response to oxidized LDL.
    • Oxidized LDL activates key inflammatory pathways, promoting plaque development.
    • HDL's enzymatic activity may offer protection against atherosclerosis by neutralizing harmful oxidized lipids.