Abstract
The discovery of lipoprotein(a) [Lp(a)] in 1963, followed by a more detailed biochemical characterisation in the 1970s, introduced a dazzling new lipoprotein composed of two components: an apolipoprotein (apo)B-containing low-density lipoprotein (LDL)-like particle, covalently linked to a plasminogen-like glycoprotein apo(a). 1 Utermann G The mysteries of lipoprotein(a). Science. 1989; 246: 904-910 Crossref PubMed Scopus (1090) Google Scholar During the next three decades, genetic approaches greatly advanced the understanding of this particle. Lp(a) is subject to tight genetic control, with more than 90% of its variance residing in the LPA gene encoding apo(a). 2 Boerwinkle E Leffert CC Lin J Lackner C Chiesa G Hobbs HH Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J Clin Invest. 1992; 90: 52-60 Crossref PubMed Scopus (812) Google Scholar Subsequent genetic studies, 3 Kronenberg F Utermann G Lipoprotein(a): resurrected by genetics. J Intern Med. 2013; 273: 6-30 Crossref PubMed Scopus (315) Google Scholar including a genome-wide association study, a candidate gene approach, and a mendelian randomisation study, identified Lp(a) as a causal, independent risk factor for cardiovascular disease. Antisense therapy targeting apolipoprotein(a): a randomised, double-blind, placebo-controlled phase 1 studyISIS-APO(a)Rx results in potent, dose-dependent, selective reductions of plasma Lp(a). The safety and tolerability support continued clinical development of ISIS-APO(a)Rx as a potential therapeutic drug to reduce the risk of cardiovascular disease and calcific aortic valve stenosis in patients with elevated Lp(a) concentration. Full-Text PDF
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