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  • Lipoprotein(a)-the crossroads of atherosclerosis, atherothrombosis and inflammation [Elektronski vir]
    Ugovšek, Sabina ; Šebeštjen, Miran
    Increased lipoprotein(a) (Lp(a)) levels are an independent predictor of coronary artery disease (CAD), degenerative aortic stenosis (DAS), and heart failure independent of CAD and DAS. Lp(a) levels ... are genetically determinated in an autosomal dominant mode, with great intra- and inter-ethnic diversity. Most variations in Lp(a) levels arise from genetic variations of the gene that encodes the apolipoprotein(a) component of Lp(a), the LPA gene. LPA is located on the long arm of chromosome 6, within region 6q2.6–2.7. Lp(a) levels increase cardiovascular risk through several unrelated mechanisms. Lp(a) quantitatively carries all of the atherogenic risk of low-density lipoprotein cholesterol, although it is even more prone to oxidation and penetration through endothelia to promote the production of foam cells. The thrombogenic properties of Lp(a) result from the homology between apolipoprotein(a) and plasminogen, which compete for the same binding sites on endothelial cells to inhibit fibrinolysis and promote intravascular thrombosis. LPA has up to 70% homology with the human plasminogen gene. Oxidized phospholipids promote differentiation of pro-inflammatory macrophages that secrete pro-inflammatory cytokines (e. g., interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α). The aim of this review is to define which of these mechanisms of Lp(a) is predominant in different groups of patients.
    Vir: Biomolecules [Elektronski vir]. - ISSN 2218-273X (Vol. 12, iss. 1, 2022, str. 1-14)
    Vrsta gradiva - e-članek ; neleposlovje za odrasle
    Leto - 2022
    Jezik - angleški
    COBISS.SI-ID - 91854339

    Povezava(-e):

    https://www.mdpi.com/2218-273X/12/1/26
    Repozitorij Univerze v Ljubljani – RUL
    DOI

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