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Updated: Jul 10, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
07:29

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

Published on: October 12, 2017

Myeloperoxidase and inflammatory proteins: pathways for generating dysfunctional high-density lipoprotein in humans

Tomás Vaisar1, Baohai Shao, Pattie S Green

  • 1Department of Medicine, HSB-BB512, Box 356426, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195, USA.

Current Atherosclerosis Reports
|November 16, 2007
PubMed

Insights

High-density lipoprotein (HDL) becomes dysfunctional in cardiovascular disease (CVD) due to oxidation and altered protein cargo. This dysfunction may contribute to atherosclerosis and impact HDL

Area of Science:

  • Cardiovascular biology
  • Lipid metabolism
  • Inflammation research

Background:

  • High-density lipoprotein (HDL) plays a key role in reverse cholesterol transport and possesses anti-atherogenic and anti-inflammatory properties.
  • Dysfunctional HDL, particularly in individuals with cardiovascular disease (CVD), may lose its protective functions.
  • Myeloperoxidase (MPO) has been implicated in targeting HDL for oxidation, potentially leading to its dysfunction.

Purpose of the Study:

  • To investigate the mechanisms by which HDL function is altered in subjects with established CVD.
  • To identify specific protein modifications and cargo changes in HDL from CVD patients.
  • To explore the role of oxidative stress and inflammation in HDL dysfunction.

Main Methods:

  • Shotgun proteomic analysis of HDL.
  • Mass spectrometry and biochemical analyses of HDL composition.
  • Studies on HDL from subjects with established cardiovascular disease (CVD).

Main Results:

  • HDL from CVD subjects showed oxidative modifications and altered protein composition.
  • Myeloperoxidase (MPO) was identified as a key enzyme targeting HDL for oxidation, impairing cholesterol efflux.
  • HDL(3) from CVD patients was selectively enriched in apolipoprotein E and other inflammatory proteins.

Conclusions:

  • Oxidative modifications and changes in protein cargo render HDL dysfunctional in CVD.
  • These alterations in HDL may serve as both biomarkers and mediators of cardiovascular disease.
  • Targeting HDL dysfunction presents a potential therapeutic strategy for CVD.

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