Apolipoproteins and atherosclerosis. Apolipoprotein E and apolipoprotein(a) as candidate genes of premature development of atherosclerosis
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, přehledy
PubMed
10984073
Knihovny.cz E-zdroje
- MeSH
- alely MeSH
- Alzheimerova nemoc krev genetika metabolismus MeSH
- apolipoproteiny E krev chemie genetika metabolismus MeSH
- apolipoproteiny krev chemie genetika metabolismus MeSH
- arterioskleróza krev epidemiologie genetika metabolismus MeSH
- genetická predispozice k nemoci MeSH
- hyperlipoproteinemie krev genetika metabolismus MeSH
- lidé MeSH
- lipoprotein (a) krev chemie genetika metabolismus MeSH
- lipoproteiny LDL metabolismus MeSH
- protein - isoformy krev chemie genetika metabolismus MeSH
- věk při počátku nemoci MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- apolipoproteiny E MeSH
- apolipoproteiny MeSH
- lipoprotein (a) MeSH
- lipoproteiny LDL MeSH
- protein - isoformy 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.