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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:267.)
© 2005 American Heart Association, Inc.

Editorials

Apolipoprotein E and Atherosclerosis

Beyond Lipid Effect

Jean Davignon

From the Hyperlipidemia and Atherosclerosis Research Group, Clinical Research Institute of Montreal, Canada.

Correspondence to Jean Davignon, IRCM, 110 Pine Ave. West, Montreal, QC, H2W 1R7. E-mail jean.davignon@ircm.qc.ca

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

In humans, apolipoprotein E (apoE) is a polymorphic multifunctional protein.¹ It is coded by three alleles (2, 3, 4) of a modulator gene (level, variability, and susceptibility gene) at the apoE locus on chromosome 19, determining six apoE genotypes and plasma phenotypes. Its pleiotropic effects are exerted on plasma lipoprotein metabolism, coagulation, oxidative processes, macrophage, glial cell and neuronal cell homeostasis, adrenal function, central nervous system physiology, inflammation, and cell proliferation.^2,3 ApoE polymorphism modulates susceptibility to many diseases. It is, however, particularly notorious for its role in neurodegenerative disorders⁴ and atherosclerotic arterial disease.^5,6 The 4 allele (phenotypes E4/4 and E4/3) that is associated with higher low density lipoprotein cholesterol (LDL-C) is considered proatherogenic, whereas the presence of the 2 allele (E3/2, E2/2), being associated with lower LDL-C levels, is deemed to have the opposite effect (although it may be associated with increased plasma triglycerides and lipoprotein remnants). This simple equation, however, is an oversimplification because these properties are subject to many environmental and genetic influences. ApoE has allele- and gender-dependent effects on reverse cholesterol transport, platelet aggregation, and oxidative processes that are likely to affect the overall atherogenic potential ascribed to modulation of lipoprotein metabolism.^2,3,6 Notwithstanding the context dependency, a recent meta-analysis fully supports the presence of the 4 allele as a significant risk factor for coronary artery disease.⁷ Several mechanisms have been evoked to link apoE with atherosclerosis, but the relationship is not fully unraveled in humans. Nevertheless, some apoE mimetic peptides that promote LDL clearance are currently . . . [Full Text of this Article]

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