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High-density lipoprotein: is it always atheroprotective?

Benjamin J Ansell1, Gregg C Fonarow, Alan M Fogelman

  • 1Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 100 UCLA Medical Plaza, Suite 525, Los Angeles, CA 90095, USA. bansell@mednet.ucla.edu

Current Atherosclerosis Reports
|August 12, 2006
PubMed
Summary

High-density lipoproteins (HDL) typically protect against atherosclerosis. However, modified HDL can paradoxically promote vascular inflammation and LDL oxidation, especially during chronic inflammation.

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Area of Science:

  • Cardiovascular Science
  • Lipid Metabolism
  • Inflammation Biology

Background:

  • High-density lipoproteins (HDL) are known for atheroprotective functions like reverse cholesterol transport, antioxidant, anti-inflammatory, and antithrombotic effects.
  • A well-established inverse relationship exists between HDL cholesterol levels and atherosclerosis prevalence across diverse populations.
  • Emerging evidence suggests HDL may lose its protective role and even promote vascular inflammation and LDL oxidation under certain conditions.

Purpose of the Study:

  • To investigate the circumstances under which HDL may exhibit paradoxical pro-inflammatory and pro-oxidative effects.
  • To explore the specific chemical modifications and structural alterations within HDL associated with this atherogenic phenotype.
  • To understand the link between proinflammatory HDL and chronic systemic inflammatory conditions, including atherosclerosis.

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Main Methods:

  • Analysis of recent studies examining HDL chemical modifications.
  • Investigation of structural changes within HDL particles.
  • Correlation of proinflammatory HDL phenotype with chronic inflammatory states.

Main Results:

  • Identification of specific HDL modifications and structural changes linked to a pro-inflammatory phenotype.
  • Demonstration that modified HDL can promote vascular inflammation.
  • Association of proinflammatory HDL with conditions characterized by chronic systemic inflammation, such as atherosclerosis.

Conclusions:

  • HDL's atheroprotective role is not absolute and can be compromised by specific modifications.
  • Modified HDL particles can paradoxically contribute to vascular inflammation and low-density lipoprotein oxidation.
  • The presence of proinflammatory HDL is linked to chronic inflammatory diseases, highlighting a shift in HDL's function.