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. 2021 Jul 19;30(1):15–24. doi: 10.1007/s12471-021-01600-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Mechanisms of action of the discussed lipid-lowering therapies. Pelacarsen inhibits apolipoprotein(a) (apo[a]). Inclisiran prevents translation of proprotein convertase subtilisin kexin type 9 (PCSK9) mRNA. PCSK9i (inhibiting) monoclonal antibodies (mab) inhibit PCSK9 binding to low-density lipoprotein receptor (LDLR). Fibrates mainly prevent synthesis of triglycerides (TG) and very-low-density lipoprotein (VLDL) production in the liver. Bempedoic acid prevents cholesterol synthesis by inhibition of adenosine triphosphate citrate lyase (ACL). Statins block 3‑hydroxy-3-methylglutaryl coenzyme reductase (HMGCR). Angiopoetin-like 3 protein inhibitors (ANGPTL3i), fibrates and apoC-III inhibitors (apoC-IIIi) enhance lipoprotein lipase (LPL) function. Ezetimibe targets Niemann-Pick C1-like 1 protein (NPC1L1), inhibiting transport of sterols into enterocytes. Created with BioRender (BioRender.com). CoA coenzyme A, IDL intermediate-density lipoprotein, Lp(a) lipoprotein(a)