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Clinical Chemistry and Laboratory Medicine (CCLM)

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Volume 45, Issue 12 (Dec 2007)


Hyperhomocysteinemia and high-density lipoprotein metabolism in cardiovascular disease

Dan Liao
  • 1Department of Surgery, Baylor College of Medicine, Houston, TX, USA
/ Xiaofeng Yang
  • 2Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, USA
/ Hong Wang
  • 3Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, USA


Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular disease (CVD) and the underlying mechanism is unclear. We and others have reported that homocysteine (Hcy) is inversely correlated with plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein AI (apoA-I) in patients with coronary heart disease (CHD). We confirmed this negative correlation in mice with targeted deletions of the genes for apolipoprotein E (apoE) and cystathionine β-synthase (CBS). Severe HHcy (plasma Hcy 210 μmol/L) accelerates spontaneous arthrosclerosis in the CBS−/−/apoE−/− mice, reduces the concentration of circulating HDL, apoA-I, and large HDL particles, inhibits HDL function, and enhances HDL-C clearance. We have demonstrated further that Hcy (0.5–2 mmol/L) reduces apoA-I protein synthesis and secretion, but not RNA transcription in mouse primary hepatocytes. A different mechanism was proposed based on studies using the HepG2 cells showing that Hcy (5–10 mmol/L) inhibits apoA-I transcription via peroxisome proliferator-activated receptor-α (PPARα)-inhibition-dependent and -independent mechanisms. These studies suggest that Hcy-induced HDL-C and apoA-I inhibition represent a novel mechanism by which Hcy induces atherosclerotic CVD.

Clin Chem Lab Med 2007;45:1652–9.

Keywords: atherosclerotic cardiovascular disease; high-density lipoprotein metabolism; hyperhomocysteinemia

About the article

Corresponding author: Hong Wang, Department of Pharmacology, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA Phone: +1-215-707-5986, Fax: +1-215-707-7068,

Received: 2007-09-04

Accepted: 2007-10-02

Published in Print: 2007-12-01

Citation Information: Clinical Chemical Laboratory Medicine, ISSN (Online) 14374331, ISSN (Print) 14346621, DOI: https://doi.org/10.1515/CCLM.2007.358. Export Citation

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