The role of dysfunctional HDL in atherosclerosis

Mohamad Navab1, Srinivasa T Reddy, Brian J Van Lenten

  • 1Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA. mnavab@mednet.ucla.edu

Journal of Lipid Research
|October 29, 2008
PubMed

Insights

Dysfunctional high-density lipoprotein (HDL) impairs reverse cholesterol transport and promotes inflammation, particularly in atherosclerosis. ApoA-I mimetic peptides show promise in restoring HDL function by binding oxidized lipids.

Area of Science:

  • Cardiovascular Science
  • Lipid Metabolism
  • Inflammation Biology

Background:

  • High-density lipoprotein (HDL) plays a crucial role in lipid metabolism and possesses anti-inflammatory properties.
  • Dysfunctional HDL is implicated in chronic inflammatory conditions, notably atherosclerosis.
  • Loss of HDL's anti-inflammatory function often parallels impaired reverse cholesterol transport.

Purpose of the Study:

  • To review the role of HDL in regulating low-density lipoprotein (LDL) oxidation and LDL-induced inflammation.
  • To explore the mechanisms underlying HDL dysfunction in inflammatory diseases.
  • To discuss potential therapeutic strategies for restoring HDL function.

Main Methods:

  • Literature review of studies on HDL function, LDL oxidation, and inflammation.
  • Analysis of data from animal models and human studies of atherosclerosis.
  • Examination of the effects of apoA-I mimetic peptides on HDL function.

Main Results:

  • Dysfunctional HDL is associated with increased LDL oxidation and inflammation in atherosclerosis.
  • Impaired reverse cholesterol transport is a hallmark of dysfunctional HDL.
  • ApoA-I mimetic peptides demonstrate potential in improving HDL function by targeting oxidized lipids.

Conclusions:

  • HDL dysfunction contributes significantly to the pathogenesis of atherosclerosis.
  • Restoring HDL's anti-inflammatory and cholesterol-efflux capacities is a key therapeutic goal.
  • ApoA-I mimetic peptides represent a promising therapeutic avenue for managing HDL dysfunction.

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