Apolipoproteins and atherosclerosis. Apolipoprotein E and apolipoprotein(a) as candidate genes of premature development of atherosclerosis
Language English Country Czech Republic Media print
Document type Journal Article, Review
PubMed
10984073
Knihovny.cz E-resources
- MeSH
- Alleles MeSH
- Alzheimer Disease blood genetics metabolism MeSH
- Apolipoproteins E blood chemistry genetics metabolism MeSH
- Apolipoproteins blood chemistry genetics metabolism MeSH
- Arteriosclerosis blood epidemiology genetics metabolism MeSH
- Genetic Predisposition to Disease MeSH
- Hyperlipoproteinemias blood genetics metabolism MeSH
- Humans MeSH
- Lipoprotein(a) blood chemistry genetics metabolism MeSH
- Lipoproteins, LDL metabolism MeSH
- Protein Isoforms blood chemistry genetics metabolism MeSH
- Age of Onset MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Apolipoproteins E MeSH
- Apolipoproteins MeSH
- Lipoprotein(a) MeSH
- Lipoproteins, LDL MeSH
- Protein Isoforms MeSH
Apolipoprotein E (apoE) is a plasma lipoprotein which plays a basic role in the degradation of particles rich in cholesterol and triglycerides. It is able to bind to LDL receptors, but also to receptors for chylomicron remnants. There are three major apoE isoforms, E2, E3, and E4. Their role in lipoprotein metabolism is related to their affinity for receptors. Allele E3 is predominant and apoE3 affects metabolism of lipoproteins in a standard way. When compared to allele E3, allele E2 is associated with lower LDL levels, whereas allele E4 with higher LDL levels. This has an impact on the progression of atherosclerosis. Allele E2 exhibits a protective role, whereas allele E4 is associated with a high risk factor. Lipoprotein(a) [Lp(a)] is a plasma lipoprotein, consisting of apolipoprotein(a), linked by a covalent bond with the LDL particle. Increased Lp(a) levels are associated with an increased incidence of diseases based on atherosclerosis, namely the ischemic heart disease. Another effect of Lp(a) is its competition with plasminogen, resulting in a decrease of fibrinolysis and thrombogenic activity. ApoE and Lp(a) are independent risk factors for premature development of atherosclerosis and therefore can be considered as candidate genes of premature atherosclerosis.