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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Lipoprotein(a): from molecules to therapeutics
Valmore Bermúdez1, Nailet Arráiz, Daniel Aparicio
1Endocrine and Metabolic Diseases Research Center, University of Zulia, School of Medicine, Maracaibo, Venezuela. valmore@gmail.com
American Journal of Therapeutics
|May 19, 2010
Summary
Lipoprotein (a) [Lp(a)] is a genetic risk factor for cardiovascular disease. Current treatments show limited success in reducing high Lp(a) plasma levels, necessitating further research.
Area of Science:
- Biochemistry
- Genetics
- Cardiology
Background:
- Lipoprotein (a) [Lp(a)], discovered in 1963, possesses unique apolipoprotein(a) linked to Apo B-100.
- Structural homology with plasminogen confers atherogenic and atherothrombotic properties.
- Elevated Lp(a) levels are strongly associated with coronary artery and cerebral vascular disorders.
Purpose of the Study:
- To review the significance of Lipoprotein (a) [Lp(a)] in cardiovascular health.
- To explore the genetic basis and population variations of Lp(a) levels.
- To assess the efficacy of current therapeutic interventions for hyper-Lp(a).
Main Methods:
- Review of case control studies and genetic research on Lp(a).
- Analysis of the genetic transmission and polymorphic gene variations influencing serum Lp(a) levels.
- Evaluation of various drug treatments and lifestyle interventions aimed at reducing Lp(a).
Main Results:
- Hyper-Lp(a) is a confirmed risk factor for premature cardiovascular disease.
- Lp(a) levels exhibit significant inter-individual, sex, and population variations due to genetic factors.
- Despite various interventions, no consistently effective therapeutic option for reducing plasma Lp(a) has been established.
Conclusions:
- Lipoprotein (a) [Lp(a)] is a significant, genetically determined risk factor for cardiovascular and cerebrovascular diseases.
- Understanding the genetic variations in Lp(a) is crucial for risk assessment.
- Effective therapeutic strategies for lowering Lp(a) remain a critical unmet need in clinical practice.
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