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Updated: Jul 20, 2025

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
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Lipoprotein(a) in clinical practice: A guide for the clinician
Chayakrit Krittanawong1, Neil Sagar Maitra2, Adham H El-Sherbini3
1Cardiology Division, NYU Langone Health and NYU School of Medicine, New York, NY, United States of America.
Insights
Serum lipoprotein(a) (Lp(a)) is a key risk factor for cardiovascular disease (CVD). Emerging research explores Lp(a) genetics, mechanisms, and new therapies to lower Lp(a) and reduce CVD risk.
Area of Science:
- Cardiology
- Genetics
- Biochemistry
Background:
- Cardiovascular disease (CVD) is a leading global cause of mortality.
- Serum lipoprotein(a) (Lp(a)) is an independent and causative risk factor for atherosclerotic CVD and calcific aortic valvular disease.
Purpose of the Study:
- To review recent advances in understanding lipoprotein(a) (Lp(a)).
- To discuss current management strategies and emerging therapies for Lp(a) reduction.
- To explore future directions in targeting Lp(a) for CVD prevention.
Main Methods:
- Review of recent scientific literature on Lp(a).
- Analysis of genetic polymorphisms in the LPA gene.
- Examination of real-world data on risk factor interactions.
- Evaluation of metabolic pathway targets for Lp(a) lowering.
Main Results:
- Novel insights into Lp(a) epidemiology and pathogenic mechanisms.
- Identification of genetic factors influencing Lp(a) levels.
- Understanding of Lp(a) interactions with other cardiovascular risk factors.
- Emerging therapeutic targets for Lp(a) reduction.
Conclusions:
- Lp(a) is a critical target for CVD risk reduction.
- Advances in understanding Lp(a) pave the way for new treatment strategies.
- Future research should focus on effective Lp(a)-lowering therapies.
Abstract:
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Serum lipoprotein(a) (Lp(a)) has been shown to be an independent and causative risk factor for atherosclerotic CVD and calcific aortic valvular disease. Lp(a) continues to be studied, with emerging insights into the epidemiology of CVD with respect to Lp(a), pathogenic mechanisms of Lp(a) and strategies to mitigate disease. There have been novel insights into genetic polymorphisms of the LPA gene, interactions between concomitant risk factors and Lp(a) based on real-world data, and metabolic pathway targets for Lp(a) reduction. This review highlights these recent advances in our understanding of Lp(a) and discusses management strategies as recommended by cardiovascular professional societies, emerging therapies for lowering Lp(a), and future directions in targeting Lp(a) to reduce CVD.
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