Lipoprotein-associated phospholipase A2 (Lp-PLA2)
- 50kDa, Ca-insensitive lipase
- Produced predominantly by macrophages
- An enzyme that resides mainly on LDL in human plasma
- Distinct from secretory phospholipase A2 (sPLA2)
- Levels are not affected by acute systemic inflammatory conditions
- Intra-individual variability is similar to other lipid parameters, such as LDL-C and TC
Lp-PLA2 is Related to Atherosclerosis
- Elevated plasma levels correlate with CHD and ischemic stroke risk
- Highly up-regulated in atherosclerotic plaques
- The enzyme Lp-PLA2 is implicated in formation of inflamed, rupture-prone plaque
- Responsible for generating two pro-inflammatory mediators during LDL oxidation
- lysophosphatidylcholine (Lyso-PC)
- oxidized fatty acid (OxFA)
- In pre-clinical animal studies, inhibition of the enzyme attenuates the inflammatory process and slows atherosclerotic disease progression
Pro-atherogenic Activities of Lysophosphatidylcholine (Lyso-PC)
- Impairment of endothelium dependent relaxation
- Induces expression of vascular adhesion molecules
- Chemoattractant for inflammatory cells
- Up-regulation of Cytokines and CD 40 Ligand
- Stimulation of macrophage proliferation
- Cytotoxic to vascular smooth muscle cells
Lp-PLA2 is a Potential Therapeutic Target for Anti-Atherosclerotic Treatments
- GlaxoSmithKline (GSK) is currently developing small molecule inhibitors as potential treatments for atherosclerotic disease
- Currently available medications that are known to reduce cardiovascular events, such as statins and fibrates, are also known to reduce Lp-PLA2 levels
Lp-PLA2 and
Vulnerable Plaque
The thin fibrous cap may burst and form a thrombotic clot that can lead to a stroke or coronary event. (Click to enlarge)
Click below to view a short animation that illustrates how Lp-PLA2 contributes to the formation of vulnerable plaque, which can cause CHD or stroke.









