Treatment with the antibiotic myriocin can halt the growth of established arterial plaques in mice, researchers report.
Myriocin kills bacteria by disrupting the formation sphingomyelin, a fatty molecule that is a key part of their cell membranes. Since sphingomyelin is also a major component of fatty plaques that can build up in blood vessels, myriocin could be a potential treatment option for atherosclerosis. In fact, some studies have shown that myriocin can suppress the development of atherosclerosis in mice fed a high-fat diet.
Taking this idea one step further, Brett Garner and colleagues aimed to determine whether myriocin could suppress or even reverse pre-existing atherosclerotic lesions. Adult transgenic mice were fed a high-fat diet for 30 days to stimulate plaque formation, at which point the mice were transferred to either a regular diet or a diet containing myriocin.
The researchers then measured lesion size and found that myriocin significantly inhibited the progress of established atherosclerosis, which coincided with decreases in the concentration of sphingomyelin, cholesterol, and triglycerides in the blood. Although the researchers did not observe any shrinkage of lesions, myriocin still could offer therapeutic benefits to individuals with early-stage atherosclerosis
Corresponding Author: Brett Garner, Prince of Wales Medical Research Institute, Randwick, Australia; Tel: +61 (02) 9399 1024, e-mail: firstname.lastname@example.org
Making Statins Even Better
Statin drugs are helping many people lower their cholesterol, but a new study reveals that statins actually increase the production of another protein that limits their benefit.
Proprotein convertase type 9 (PCSK9) has recently gained attention as a key regulator of LDL cholesterol (the “bad” cholesterol). PCSK9 degrades LDL receptors that remove LDL cholesterol (LDL-C) from the blood; mutations that result in extra PCSK9 activity produce familial hypercholesterolemia, while mutations causing less PCSK9 activity lower LDL-C and cardiovascular risk.
Studies in mice have indicated that statins may increase PCSK9 expression, so Robert Konrad and colleagues studied the effect of atorvastatin (Lipitor) or placebo on PCSK9 levels in humans. After 16 weeks of treatment, 40 mg/day atorvastatin increased circulating PCSK9 levels by 34% over placebo, while decreasing LDL-C levels by 42%. In comparison, a 10 mg/day dosage did not increase PCSK9 levels at all, yet still reduced LDL-C by 30%.
The researchers note these results, although preliminary, suggest that adding a PCSK9 inhibitor to statin therapy could be an approach to further decrease LDL-C levels in patients unable to reach desired results on statin therapy alone, or to effectively lower the dosage in patients who experience unwanted statin side effects.
Corresponding Author: Robert Konrad, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN; Phone: 317-655-9290, email:email@example.com
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