Abstract
The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have potent anti-inflammatory, vasodilatory and anti-platelet effects that are independent of the lipid-lowering effects. These non-lipid-lowering or pleiotropic effects are dependent on HMG-CoA reductase inhibition in tissues other than the liver. In animal models, high-dose statins upregulate cytosolic phospholipase A 2 and cyclooxygenase-2, leading to increased production of prostacyclin and 15-deoxy-PGJ 2. In addition, statins activate protein kinase A, which phosphorylates 5-lipoxygenase, resulting in decreased production of the pro-inflammatory leukotrienes and increased production of 15-epi-lipoxin A4, an eicosanoid with potent anti-inflammatory and inflammation-resolution properties. It is unclear, however, whether these effects occur in the clinical setting and whether these effects (partially) explain the anti-inflammatory effects of statins in patients.
Original language | English (US) |
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Pages (from-to) | 135-139 |
Number of pages | 5 |
Journal | Current Atherosclerosis Reports |
Volume | 14 |
Issue number | 2 |
DOIs | |
State | Published - Apr 2012 |
Keywords
- 5-lipooxygenase
- Arachidonic acid
- Aspirin
- Cyclooxygenase-2
- Eicosanoids
- Inflammation
- LDL cholesterol
- Pleiotropic effects
- Prostacyclin
- Protein kinase A (PKA)
- Statins
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine