Statins could also reduce plaque in arteries

Washington, Dec 14 (ANI): Researchers have discovered the molecular phenomenon that cholesterol-lowering drugs called statins go through to promote the breakdown of plaque in the arteries.

The findings by NYU Langone Medical Centre researchers support a large clinical study that recently showed patients taking high-doses of the cholesterol-lowering medications not only reduced their cholesterol levels but also reduced the amount of plaque in their arteries.

However, until now researchers did not fully understand how statins could reduce atherosclerosis, the accumulation of fat and cholesterol that hardens into plaque in arteries, a major cause of mortality in Western countries.

High blood cholesterol is a major culprit in atherosclerosis. As a result of narrowing arteries, blood clots can form or plaque can break off causing blockages in vessels. This can lead to a potentially fatal heart attack or stroke.

"Our new research shows statins actually promote the regression of atherosclerosis by altering the expression of a specific cell surface receptor within plaque cells," said co-author of the study, Edward Fisher, MD, PhD, Leon H. Charney Professor of Cardiovascular Medicine and director of the Marc and Ruti Bell Vascular Biology Program at NYU Langone Medical Center.

"This molecular phenomenon helps dissolve plaque by expelling coronary artery disease-causing cells from the plaque lining the arteries," he explained.

In the study, researchers show in mouse models that statins activate the cell surface protein receptor C-C chemokine receptor type 7 (CCR7), which in turn activates a cell-signaling pathway forcing macrophages out of plaque.

"Our experimental findings indicate that statins, in addition to lowering LDL cholesterol, have clinical benefits of accelerating plaque regression by a newly discovered mechanism," said co-author Michael Garabedian, PhD, Professor, Department of Microbiology and Urology at NYU Langone Medical Center.

The study was published online by the journal PLoS One on December 6, 2011. (ANI)