Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

Author:

Jawi Motasim M.123ORCID,Frohlich Jiri14,Chan Sammy Y.15

Affiliation:

1. Healthy Heart Program, St. Paul’s Hospital, Vancouver V6Z 1Y6, Canada

2. Division of Experimental Medicine, Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver V5Z 1M9, Canada

3. Department of Clinical PhysiologyCorrection: Department of Physiology, University of Jeddah, P.O. Box: 24, Jeddah 21959, Saudi Arabia

4. Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada

5. Department of Medicine, Division of Cardiology, University of British Columbia, Vancouver V5Z 1M9, Canada

Abstract

Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

Publisher

Hindawi Limited

Subject

Biochemistry

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