A research team has shown that a nanotherapeutic medicine can halt the growth of artery plaque cells resulting in the fast reduction of the inflammation that may cause a heart attack or stroke, according to a study led by researchers from Icahn School of Medicine at Mount Sinai in New York City and published online on April 3, 2015 in an open-access article in Science Advances. The article is titled “Inhibiting Macrophage Proliferation Suppresses Atherosclerotic Plaque Inflammation.” "In just one week, our novel cell proliferation-specific approach successfully suppressed atherosclerotic plaque growth and inflammation in mice engineered to mimic human vascular disease," says lead study author Jun Tang, M.S., a Ph.D. student at Icahn School of Medicine at Mount Sinai. “Atherosclerosis is a major cause of death around the globe, and our nanomedicine strategy promises to offer a new way to reduce the number of heart attacks and strokes." Building upon a recent discovery by their Massachusetts General Hospital (MGH) research collaborators that macrophage proliferation dictates atherosclerosis-related vessel wall inflammation, the Mount Sinai research team applied a nanomedicine strategy with a molecule of "good cholesterol," or high-density lipoprotein (HDL), a naturally occurring shuttle that travels from the liver to arteries. The research team took advantage of HDL's natural travel routes, loading it with the widely-used cholesterol-lowering medication called simvastatin (Zocor), which it shuttles into arterial walls. The simvastatin-loaded nanoparticles, named S-HDL, work by targeting inflamed immune cells called macrophages within high-risk arterial plaques. These macrophages become laden with cholesterol and start proliferating in plaques, thereby increasing inflammation.
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