Dysfunctional high-density lipoprotein

Hong Feng, Xiang An Li

Research output: Contribution to journalReview articlepeer-review

42 Scopus citations

Abstract

PURPOSE OF REVIEW: To address the progress of the investigation on dysfunctional high-density lipoprotein (HDL). RECENT FINDINGS: HDL is generally considered to be an independent protective factor against cardiovascular disease. However, emerging evidence indicates that HDL can be modified under certain circumstances and lose its protective effect or even become atherogenic. The underlying mechanisms responsible for generating the dysfunctional HDL and the chemical and structural changes of HDL remain largely unknown. Recent studies focus on the role of myeloperoxidase in generating oxidants as participants in rendering HDL dysfunctional in vivo. Myeloperoxidase modifies HDL in humans by oxidation of specific amino acid residues in apolipoprotein A-I, which impairs cholesterol efflux through ATP-binding cassette transporter A1 and contributes to atherogenesis. SUMMARY: HDL may not always be atheroprotective and can be atherogenic paradoxically under certain conditions. The mechanisms responsible for generating the dysfunctional HDL remain largely unknown. Recent data suggest that myeloperoxidase-associated modification of HDL may be one of the mechanisms. Further studies are needed to investigate the in-vivo mechanisms of HDL modification and identify therapeutic approaches aiming at controlling HDL modification.

Original languageEnglish
Pages (from-to)156-162
Number of pages7
JournalCurrent Opinion in Endocrinology, Diabetes and Obesity
Volume16
Issue number2
DOIs
StatePublished - Apr 2009

Keywords

  • Apolipoprotein A-I
  • Cardiovascular disease
  • High-density lipoprotein
  • Lipoprotein
  • Myeloperoxidase

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

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