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Updated: Jun 21, 2026
06:47
Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Lipoprotein-associated phospholipase A(2) and atherosclerosis
Robert L Wilensky1, Colin H Macphee
1Cardiovascular Division, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. robert.wilensky@uphs.upenn.edu
Current Opinion in Lipidology
|August 12, 2009
Summary
Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is linked to cardiovascular events. Targeting Lp-PLA2 may stabilize atherosclerotic plaques by reducing inflammation and cell death.
Area of Science:
- Cardiovascular Medicine
- Inflammation Biology
- Lipid Metabolism
Background:
- Elevated lipoprotein-associated phospholipase A2 (Lp-PLA2) mass or activity correlates with increased risk of cardiac death, myocardial infarction, acute coronary syndromes, and ischemic stroke.
- Emerging data highlight Lp-PLA2's role in the progression of advanced coronary artery disease, potentially linking lipid metabolism and vascular inflammation.
Purpose of the Study:
- To review the role of Lp-PLA2 in the development and progression of atherosclerosis.
- To explore the potential of selective Lp-PLA2 inhibition as a therapeutic strategy for advanced, unstable atherosclerosis.
Main Methods:
- Review of recent scientific literature and clinical data concerning Lp-PLA2 function and therapeutic inhibition.
- Analysis of Lp-PLA2's enzymatic activity, its products, and their impact on atherosclerotic plaque development.
Main Results:
- Lp-PLA2 cleaves oxidized phospholipids, generating pro-inflammatory mediators that promote atherosclerotic necrotic core formation.
- These mediators recruit and activate leukocytes, induce macrophage apoptosis, and hinder clearance of dead cells, contributing to plaque instability.
- Selective Lp-PLA2 inhibition has shown potential in reducing necrotic core development and stabilizing atherosclerotic plaques.
Conclusions:
- Immune pathways are critical in high-risk atherosclerosis, with persistent macrophage apoptosis playing a significant role.
- Lp-PLA2 contributes to this inflammatory response through its effects on macrophage apoptosis.
- Selective Lp-PLA2 inhibition is a potential therapeutic approach to mitigate necrotic core progression and reduce adverse clinical outcomes in advanced atherosclerosis.
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