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Updated: Jan 26, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Biology, pathophysiology and current therapies that affect lipoprotein (a) levels
Thampi Rawther1, Fatiha Tabet1
1School of Medical Sciences, Faculty of Medicine, UNSW Sydney, Sydney, NSW 2052, Australia.
Insights
Elevated Lipoprotein (a) [Lp(a)] is a genetic risk factor for cardiovascular disease. This review explores Lp(a) biology and its reduction via lipid-lowering therapies like statins and PCSK9 inhibitors.
Area of Science:
- Cardiology
- Genetics
- Pharmacology
Background:
- Lipoprotein (a) [Lp(a)] is a recognized genetic risk factor for cardiovascular and calcific aortic valve diseases.
- High prevalence of elevated Lp(a) highlights knowledge gaps in its biology and treatment.
- Lp(a) levels are genetically determined and unresponsive to lifestyle modifications.
Purpose of the Study:
- To review current understanding of Lipoprotein (a) [Lp(a)] biology, pathophysiology, and metabolism.
- To summarize the efficacy of various lipid-lowering therapies in reducing Lp(a) levels.
- To consolidate knowledge on Lp(a) response to statins, apheresis, PCSK9 inhibitors, CETP inhibitors, and ASOs.
Main Methods:
- Literature review of current scientific knowledge on Lp(a).
- Analysis of studies investigating Lp(a) reduction strategies.
- Synthesis of data on Lp(a) response to different therapeutic classes.
Main Results:
- Lp(a) is a significant independent risk factor for cardiovascular disease.
- Plasma Lp(a) levels are primarily genetically determined.
- Various lipid-lowering therapies demonstrate differential effects on Lp(a) levels.
Conclusions:
- Further research into Lp(a) biology and pathophysiology is warranted.
- Targeting Lp(a) represents a potential therapeutic strategy for cardiovascular disease prevention.
- Understanding Lp(a) response to different treatments is crucial for clinical application.
Abstract:
Lipoprotein (a) [Lp(a)] has recently emerged as a causal, independent and genetic risk factor for cardiovascular disease and calcific aortic valve disease. Given the high incidence of elevated Lp(a) among the general population, significant gaps in the knowledge of Lp(a) biology, pathophysiology and current therapies affecting Lp(a) reduction exist. As plasma Lp(a) levels are genetically determined and insensible to diet, exercise and lifestyle changes, lipid-lowering therapies seem to be the solution to lower elevated Lp(a) levels. This review summarises the current knowledge of Lp(a) structure, metabolism, catabolism, pathophysiology, and Lp(a) response to statins, lipid apheresis, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, cholesterol esterase transferase protein (CETP) inhibitors and antisense oligonucleotides (ASOs).
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