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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Tate, Jillian R. / Tsongalis, Gregory J.

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Hyperhomocysteinemia and high-density lipoprotein metabolism in cardiovascular disease

Dan Liao1 / Xiaofeng Yang2 / Hong Wang3

1Department of Surgery, Baylor College of Medicine, Houston, TX, USA

2Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, USA

3Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, USA

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,

Citation Information: Clinical Chemical Laboratory Medicine. Volume 45, Issue 12, Pages 1652–1659, ISSN (Online) 14374331, ISSN (Print) 14346621, DOI: 10.1515/CCLM.2007.358, December 2007

Publication History

Received:
2007-09-04
Accepted:
2007-10-02

Abstract

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

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