Cited by 1,981Lipoproteins and Cardiovascular HealthLipid metabolism and disordersCholesterol and Lipid Metabolism

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Apolipoprotein E polymorphism and atherosclerosis.

Davignon, J, Gregg, R E, Sing, C F·1988·Arteriosclerosis: An Official Journal of the American Heart Association, Inc.

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Abstract

The apo E locus contributes to determining the variation in plasma cholesterol levels of healthy and diseased populations. It also influences the expression of hyperlipidemia and appears to modulate the susceptibility to atherosclerosis in a complex multifactorial interaction. There is evidence that the presence of apo E2 is protective, whereas that of apo E4 predisposes to coronary artery disease. The burden of proof, however, lies on future, well-designed clinical trials and prospective studies. The study of the biological significance of the apo E polymorphism in humans has emphasized the importance of gene-gene and gene-environment interactions in the pathogenesis of hyperlipidemia and atherosclerosis. The apo E polymorphism involves the coding region of the apo E gene and results in alterations of the gene product which, in turn, either directly or secondarily affect the metabolic fate of the lipoprotein particles. Rapid advances in knowledge over the last decade have provided a metabolic explanation for the observation of the opposite effects of the epsilon 4 and the epsilon 2 alleles on lipoprotein levels. Apo E2 has lower receptor binding affinity which results in delayed clearance of apo E2-bearing lipoprotein particles from plasma. Apo E4 is distributed differently from apo E3 between VLDL and HDL, is degraded more rapidly than apo E3, and may enhance the catabolism of E4-bearing particles, leading to other alterations in lipoprotein metabolism which result in elevated levels of LDL. In view of the significant opposite impacts of the epsilon 4 and the epsilon 2 alleles on plasma LDL cholesterol concentrations, it is evident that determination of the apo E phenotype will become a useful adjunct to the assessment of the cardiovascular risk profile of an individual. In addition, the relationship between the epsilon 2 allele and type III hyperlipoproteinemia provides a valuable model for the study of complex genetic interactions in the pathogenesis of hyperlipidemia. The further study of apo E and its interactions shows great promise for a deeper comprehension of the pathogenesis of atherosclerosis.

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Authors: Davignon, J., Gregg, R. E., & Sing, C. F.
Affiliations: Montreal Clinical Research Institute (CA)
ORCID: Davignon, J
Gregg, R E
Sing, C F
Venue: Arteriosclerosis: An Official Journal of the American Heart Association, Inc.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1988-01
Volume: 8
Issue: 1
Pages: 1-21
ISSN: 0276-5047 (ISSN-L)
DOI: 10.1161/01.atv.8.1.1
OpenAlex: W2066644955
Cited by: 1,981
References: 98
Citations by year: 2026: 10 · 2025: 7 · 2024: 17 · 2023: 10 · 2022: 9 · 2021: 21 · 2020: 21 · 2019: 21 · 2018: 27 · 2017: 28 · 2016: 23 · 2015: 33 · 2014: 31 · 2013: 40 · 2012: 49
FWCI: 83.15
Type: journal article
Language: en
Open access: closed
Locations: Arteriosclerosis An Official Journal of the American Heart Association Inc (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (HL24489, HL-39107)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Keywords: APOE polymorphism, atherosclerosis, coronary artery disease, hyperlipidemia, LDL cholesterol, lipoprotein metabolism, gene-environment interaction, type III hyperlipoproteinemia, cardiovascular risk assessment, genetic susceptibility
MeSH terms: Alleles, Apolipoproteins, Apolipoproteins E, Arteriosclerosis, Coronary Disease, Humans, Lipids, Lipoproteins, Phenotype, Polymorphism, Genetic, Radiography, Risk Factors

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Apolipoprotein E polymorphism and atherosclerosis.

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