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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
Published on: November 10, 2017
Lipopotrein(a): from the complex metabolism to the optimal lowering drug
Francesco Di Giacomo Barbagallo1,2, Martina Berteotti3, Giosiana Bosco1,2
1Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi Hospital, University of Catania, Via Palermo 636, 95122, Catania, Italy.
Insights
Lipoprotein(a) [Lp(a)] significantly increases atherosclerotic cardiovascular disease risk. Current treatments are limited, but new therapies targeting Lp(a) show promise for reducing cardiovascular events.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle linked to increased atherosclerotic cardiovascular disease (ASCVD) risk.
- Lp(a) comprises an LDL-like particle covalently bound to apolipoprotein(a), carrying oxidized phospholipids that drive endothelial dysfunction and vascular inflammation.
Purpose of the Study:
- To review the role of Lp(a) in ASCVD pathogenesis.
- To discuss current and emerging therapeutic strategies for Lp(a) reduction.
Main Methods:
- Literature review of Lp(a) pathophysiology and therapeutic interventions.
- Analysis of genetic factors influencing Lp(a) levels.
Main Results:
- Lp(a) promotes ASCVD through lipid retention, inflammation, impaired fibrinolysis, and vascular calcification.
- Circulating Lp(a) levels are primarily determined by LPA gene variability, specifically kringle IV type 2 copy number variation.
- Lipoprotein apheresis is effective but limited; PCSK9 inhibitors offer partial reduction; novel therapies like ASOs, siRNAs, small molecules, and gene editing are under investigation.
Conclusions:
- Lp(a) is a critical determinant of residual cardiovascular risk.
- Understanding Lp(a) pathophysiology is crucial for developing targeted therapies to improve cardiovascular risk stratification and prevention.
Abstract:
Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD), including coronary artery disease, ischemic stroke, peripheral artery disease, and calcific aortic valve stenosis. Structurally, Lp(a) consists of an LDL-like particle covalently bound to apolipoprotein(a), a plasminogen-like glycoprotein that confers distinct biological properties. In particular, Lp(a) is the main circulating carrier of oxidized phospholipids, which promote endothelial dysfunction and vascular inflammation. Lp(a) contributes to vascular injury through multiple mechanisms, including lipid retention within the arterial wall, inflammatory activation, impairment of fibrinolysis, and vascular calcification. These processes contribute to plaque development and progression. Circulating Lp(a) levels are largely determined by genetic variability within the LPA gene, particularly by kringle IV type 2 copy number variation, which influences apolipoprotein(a) isoform size and secretion. Despite its clinical relevance, therapeutic options specifically targeting Lp(a) remain limited. Lipoprotein apheresis is the main available strategy for a substantial reduction in selected high-risk patients, while conventional lipid-lowering therapies have minimal effects and PCSK9 inhibitors provide only partial reductions. However, several targeted therapies are currently under investigation. Antisense oligonucleotides and small interfering RNAs reduce hepatic LPA expression and achieve marked reductions in circulating Lp(a) levels, and novel small molecule agents interfere with Lp(a) particle formation. Gene-editing strategies are a potential future approach for long-term Lp(a) reduction. In conclusion, Lp(a) is a key determinant of residual cardiovascular risk. A better understanding of its pathophysiology and the development of targeted therapies may improve cardiovascular risk stratification and prevention strategies.
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