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Updated: Dec 10, 2025

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Lipoprotein(a): a genetic marker for cardiovascular disease and target for emerging therapies
Arturo Cesaro1,2, Alessandra Schiavo1,2, Elisabetta Moscarella1,2
1Department of Translational Medical Sciences, University of Campania 'Luigi Vanvitelli', Naples.
Insights
Lipoprotein(a) [Lp(a)] is a key inherited cardiovascular risk factor. While lowering Lp(a) may reduce cardiovascular events, this requires further clinical trial validation for new targeted therapies.
Area of Science:
- Cardiology
- Lipidology
- Genetics
Background:
- Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor with proatherogenic and prothrombotic properties.
- Elevated Lp(a) is linked to atherosclerotic cardiovascular disease (ASCVD), particularly in younger individuals and those with residual risk despite optimal LDL-C.
- Genetic factors significantly influence plasma Lp(a) concentrations, highlighting its role as an inherited risk factor.
Purpose of the Study:
- To provide an updated overview of current evidence on Lp(a) as a cardiovascular risk factor.
- To review emerging therapeutic strategies specifically designed to reduce Lp(a) levels.
- To discuss the potential impact of Lp(a)-lowering therapies on cardiovascular event reduction.
Main Methods:
- Review of current scientific literature and clinical trial data on Lp(a).
- Analysis of the proatherogenic and prothrombotic mechanisms of Lp(a).
- Evaluation of existing and novel therapeutic approaches for Lp(a) reduction.
Main Results:
- Lp(a) possesses LDL-like and plasminogen-like activities contributing to atherosclerosis and thrombosis.
- Current lipid-lowering drugs have limited efficacy in reducing Lp(a).
- Randomized clinical trials are needed to confirm the hypothesis that lowering Lp(a) reduces cardiovascular events.
Conclusions:
- Lp(a) is a significant, genetically influenced cardiovascular risk factor.
- Novel Lp(a)-lowering therapies hold promise for future cardiovascular prevention strategies.
- Further research and clinical trials are essential to validate the therapeutic benefit of reducing Lp(a).
Abstract:
Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor, and growing evidence indicates its causal association with atherosclerotic disease because of the proatherogenic low-density lipoprotein (LDL)-like properties and the prothrombotic plasminogen-like activity of apolipoprotein(a) [apo(a)]. As genetics significantly influences its plasma concentration, Lp(a) is considered an inherited risk factor of atherosclerotic cardiovascular disease (ASCVD), especially in young individuals. Moreover, it has been suggested that elevated Lp(a) may significantly contribute to residual cardiovascular risk in patients with coronary artery disease and optimal LDL-C levels. Nonetheless, the fascinating hypothesis that lowering Lp(a) could reduce the risk of cardiovascular events - in primary or secondary prevention - still needs to be demonstrated by randomized clinical trials. To date, no specific Lp(a)-lowering agent has been approved for reducing the lipoprotein levels, and current lipid-lowering drugs have limited effects. In the future, emerging therapies targeting Lp(a) may offer the possibility to further investigate the relation between Lp(a) levels and cardiovascular outcomes in randomized controlled trials, ultimately leading to a new era in cardiovascular prevention. In this review, we aim to provide an updated overview of current evidence on Lp(a) as well as currently investigated therapeutic strategies that specifically address the reduction of the lipoprotein.
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