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Updated: Aug 24, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Lipoprotein(a). The bad cholesterol
1Department of Physiology, Shifa College of Medicine and Shifa International Hospital, Islamabad, Pakistan.
Insights
Lipoprotein(a) [Lp(a)] plays a role in atherosclerosis and coronary artery disease, acting as both an atherogenic and thrombogenic factor. Despite its known risks, Lp(a)
Area of Science:
- Cardiovascular Science
- Biochemistry
- Genetics
Background:
- Lipoprotein(a) [Lp(a)] is a lipoprotein particle that has been linked to cardiovascular disease.
- Its precise pathophysiological role in atherogenesis remains incompletely understood.
- Plasma levels of Lp(a) exhibit significant inter-individual variability.
Purpose of the Study:
- To review the role of Lp(a) in atherogenesis and coronary artery disease (CAD).
- To discuss the atherogenic and thrombogenic potentials of Lp(a).
- To examine Lp(a) as a predictor of CAD and current treatment limitations.
Main Methods:
- Review of prospective studies and scientific literature.
- Analysis of Lp(a) structure and function.
- Discussion of potential therapeutic strategies.
Main Results:
- Lp(a) possesses both atherogenic and thrombogenic properties due to its structure and interaction with macrophages.
- Prospective studies identify Lp(a) as a predictor of CAD, though significance varies.
- Current treatments for high Lp(a) levels are limited, with antisense RNA technology being explored.
Conclusions:
- The exact physiopathological role of Lp(a) requires further elucidation.
- The clinical utility of routine Lp(a) level assessment remains debated.
- Targeting Lp(a) presents a potential avenue for cardiovascular disease prevention.
Abstract:
The aim of this review is to highlight the role of lipoprotein(a) [Lp(a)] in atherogenesis and coronary artery disease. After 40 years from discovery, Lp(a) still remains an enigma and we are still far in understanding the pathophysiological role of Lp(a). Based on its peculiar structure, Lp(a) has both atherogenic and thrombogenic potentials as it is internalized by macrophages and has structural similarity with plasminogen. The results of the prospective studies performed over the past decade have also shown that Lp(a) is a predictor of coronary artery disease (CAD), even though some of the studies have failed to show a statistically significant difference in Lp(a) levels on subjects that subsequently developed CAD and those that did not. Within the population, the plasma levels can vary from <0.5 mg/dl to >200 mg/dl. There is currently no safe drug for long term treatment of patients with high levels of Lp(a). However, it has been proposed that there is a possibility of interfering with apolipoprotein(a) (apoA) translation by using adenovirus mediated antisense RNA technology. Despite more than 3 decades of intense scientific research, the physiopathological role of Lp(a) is still poorly understood and the extent to which Lp(a) levels should be assessed in clinical practice remain controversial until now.
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