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Andrew Carr, Statins as Anti-inflammatory Therapy in HIV Disease?, The Journal of Infectious Diseases, Volume 203, Issue 6, 15 March 2011, Pages 751–752, https://doi.org/10.1093/infdis/jiq120
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(See the article by Ganesan et al., on pages 756–764)
Statins are lipid-lowering, anti-inflammatory, and potentially antiretroviral drugs. Statins inhibit hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, which is a precursor of sterols, including cholesterol. Hepatic triglycerides and cholesterol are incorporated into very low–density lipoprotein (VLDL) and released into the circulation for delivery to peripheral tissues. Low-density lipoprotein (LDL) is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Statins lower plasma total and LDL cholesterol levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL. Multiple studies have found that statins safely prevent atherosclerotic disease, which has resulted in the widespread use of statin therapy.
Only part of the reduced incidence of cardiovascular disease with statin therapy can be explained by its lipid-lowering effect [1]. Some of the residual benefit is associated with reduction in plasma levels of the pro-inflammatory protein, C-reactive protein, which is a reduction that appears to occur independently of the effect of statin therapy on lipid levels [2–5], the mechanism of which is unknown.
