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Dysfunctional HDL: from structure-function-relationships to biomarkers.

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Low high-density lipoprotein cholesterol (HDL-C) increases cardiovascular risk. However, therapies increasing HDL-C show limited benefit, prompting a focus on HDL particle function over cholesterol levels for better cardiovascular disease treatments.

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Area of Science:

  • Cardiovascular Science
  • Lipid Metabolism
  • Atherosclerosis Research

Background:

  • Reduced high-density lipoprotein cholesterol (HDL-C) is linked to increased coronary artery disease (CAD) risk.
  • Recent trials show limited clinical benefit from therapies raising HDL-C, challenging the cholesterol-centric view.
  • Studies indicate no clear association between higher HDL-C and reduced cardiovascular events in patients with existing CAD.

Purpose of the Study:

  • To shift focus from HDL-C levels to HDL particle function and composition.
  • To explore the antiatherogenic potential and mechanisms of HDL.
  • To understand the heterogeneity and dysfunction of HDL in inflammatory conditions.

Main Methods:

  • Review of experimental and translational studies on HDL function.
  • Analysis of HDL's role in reverse cholesterol transport.
  • Investigation of HDL's effects on endothelial cells and inflammation.

Main Results:

  • HDL promotes macrophage reverse cholesterol transport and protects endothelial cells.
  • HDL from healthy subjects stimulates nitric oxide production and has anti-inflammatory effects.
  • HDL's vascular effects are heterogeneous and can be lost in chronic inflammatory disorders.

Conclusions:

  • Understanding HDL's mechanisms and altered vascular effects is crucial for HDL-targeted therapies.
  • A functional, rather than cholesterol-level-based, approach to HDL is needed.
  • Dysfunctional HDL in inflammatory conditions requires further investigation for therapeutic strategies.