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(Circulation Research. 2006;99:565.)
© 2006 American Heart Association, Inc.

Editorials

Homocysteine and Cardiovascular Disease

Is HDL the Link?

Philip J. Barter, Kerry-Anne Rye

From The Heart Research Institute, Sydney, Australia.

Correspondence to Philip J. Barter, The Heart Research Institute, 114 Pyrmont Bridge Road, Camperdown, Sydney 2050, Australia. E-mail barterp@hri.org.au

See related article, pages 598–606

Key Words: homocysteine • cardiovascular • apoA-I • HDL

An extract of the first 250 words of the full text is provided, because this article has no abstract.

An elevated plasma level of homocysteine has long been known as an independent predictor of cardiovascular disease.^1,2 However, in the absence of a clear mechanism linking homocysteine to cardiovascular disease, there has been an ongoing debate about whether this relationship is one of cause and effect or whether an elevated level of plasma homocysteine is an epiphenomenon, reflecting the presence of some other proatherogenic factor that is actually responsible for the cardiovascular disease. In the current issue of this journal, Liao et al³ suggest that the mechanistic link may be a homocysteine-induced reduction in the concentration of high density lipoproteins (HDLs).

Liao et al³ report that homocysteine reduces the concentration of HDL cholesterol in plasma by inhibiting the hepatic synthesis of apoA-I, the main HDL apolipoprotein. This conclusion supports the findings from another recent study by Mikael et al⁴ who also reported that homocysteine inhibits apoA-I synthesis. The results of these 2 studies not only explain the documented inverse correlation between the plasma concentrations of HDL cholesterol and homocysteine^5,6 but also raise the real possibility that a homocysteine-induced inhibition of apoA-I synthesis is the mechanism linking homocysteine to the development of atherosclerosis.

A low concentration of HDL cholesterol has been shown in numerous human population studies to be highly predictive of premature cardiovascular disease.^7,8 Furthermore, treatments that increase the level of HDL cholesterol in plasma in both animals^9,10 and humans^11,12 reduce the progression or even promote regression of atherosclerosis. HDLs have several properties that may contribute to their antiatherogenic potential.^13,14 . . . [Full Text of this Article]

Related Article:

Hyperhomocysteinemia Decreases Circulating High-Density Lipoprotein by Inhibiting Apolipoprotein A-I Protein Synthesis and Enhancing HDL Cholesterol Clearance

Dan Liao, Hongmei Tan, Rutai Hui, Zhaohui Li, Xiaohua Jiang, John Gaubatz, Fan Yang, William Durante, Lawrence Chan, Andrew I. Schafer, Henry J. Pownall, Xiaofeng Yang, and Hong Wang
Circ. Res. 2006 99: 598-606. [Abstract] [Full Text] [PDF]

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				M.-R. Taskinen, D. R. Sullivan, C. Ehnholm, M. Whiting, D. Zannino, R. J. Simes, A. C. Keech, P. J. Barter, and for the FIELD study investigators Relationships of HDL Cholesterol, ApoA-I, and ApoA-II With Homocysteine and Creatinine in Patients With Type 2 Diabetes Treated With Fenofibrate Arterioscler Thromb Vasc Biol, June 1, 2009; 29(6): 950 - 955. [Abstract] [Full Text] [PDF]