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The Role of Lp(a) in Atherosclerosis: An Overview

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Lipoprotein(a)

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Abstract

Epidemiological, Mendelian randomization, and genome-wide association studies (GWAS) have established that high levels of Lipoprotein(a) [Lp(a)] are causal for atherosclerotic cardiovascular disease (ASCVD). Lp(a) is an apolipoprotein B100 (apoB100)-containing particle that circulates in human plasma, distinguished by its lipid composition and presence of apolipoprotein(a) [apo(a)]. Plasma levels of Lp(a) are primarily genetically determined and vary significantly among different ethnicities. The role of Lp(a) as a contributor to atherogenic processes has been studied by various authors, but its exact pathophysiology, independent of conventional apoB injury, has not been completely described. Advancements in mass spectrometry have enhanced the ability to study Lp(a) composition further. These new tools have led to identification of novel pathways unique to Lp(a), which may explain its pathogenic nature and links to ASCVD, mainly, via the oxidized phospholipid pathway and propagation of the inflammatory cascade. In this overview, we provide brief updates on the role of Lp(a) in myocardial infarction, aortic stenosis, stroke, and peripheral artery disease, highlighting its relevance to disease outcomes, genetics, and role of potential treatments.

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Matveyenko, A., Pavlyha, M., Reyes-Soffer, G. (2023). The Role of Lp(a) in Atherosclerosis: An Overview. In: Kostner, K., Kostner, G.M., Toth, P.P. (eds) Lipoprotein(a). Contemporary Cardiology. Humana, Cham. https://doi.org/10.1007/978-3-031-24575-6_9

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