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 / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.
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Hyperhomocysteinemia and high-density lipoprotein metabolism in cardiovascular disease
- 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
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.
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