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Cholesterol-lowering medication accelerates depletion of plaque inarteries - China Decorative Butto by grass lawn





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Cholesterol-lowering medication accelerates depletion of plaque inarteries - China Decorative Butto by
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Cholesterol-lowering medication accelerates depletion of plaque inarteries - China Decorative Butto


 
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In a new study, NYU Langone Medical Center researchers havediscovered how cholesterol-lowering drugs called statins promotethe breakdown of plaque in the arteries. The study was publishedonline by the journal PLoS One on December 6, 2011. The findings support a large clinical study that recently showedpatients taking high-doses of the cholesterol-lowering medicationsnot only reduced their cholesterol levels but also reduced the amount of plaque in their arteries.However, until now researchers did not fully understand how statinscould reduce atherosclerosis, the accumulation of fat andcholesterol that hardens into plaque in arteries, a major cause ofmortality in Western countries. High blood cholesterol is a majorculprit in atherosclerosis. As a result of narrowing arteries,blood clots can form or plaque can break off causing blockages invessels.

This can lead to a potentially fatal heart attack or stroke . "Our new research shows statins actually promote the regression ofatherosclerosis by altering the expression of a specific cellsurface receptor within plaque cells," said co-author of the study,Edward Fisher, MD, PhD, Leon H. Charney Professor of CardiovascularMedicine and director of the Marc and Ruti Bell Vascular BiologyProgram at NYU Langone Medical Center. "This molecular phenomenonhelps dissolve plaque by expelling coronary artery disease-causingcells from the plaque lining the arteries." The NYU Langone study reveals how statins promote thetransformation of arterial plaques by activating a protein thatsits on the surface of macrophages, immune cells that are prevalentin plaque.

The immune system sends macrophages to clean upcholesterol deposits in arteries, but once they fill up with thebad form of cholesterol they get stuck in the arteries, triggeringthe body's inflammatory response. The bloated macrophages thenbecome major components of plaque lining artery walls. In the study, researchers show in mouse models that statinsactivate the cell surface protein receptor C-C chemokine receptortype 7 (CCR7), which in turn activates a cell-signaling pathwayforcing macrophages out of plaque. In addition, the researchersshow that macrophages only leave plaque when CCR7 is expressed.Therefore, regression of plaque is dependent on CCR7, theresearchers concluded.

The statins appeared to directly regulateand enhance CCR7 gene expression and induce macrophage cells toleave the plaque. CCR7 is a widely studied protein associated withthe migration of immune cells and its expression is a marker of thepresence of macrophages. Statins are potent inhibitors of HMG-CoA reductase, the enzyme thatplays a central role in the production of cholesterol. Statins havebeen shown to reduce the risk of cardiovascular disease and cardiacevents like heart attack. Cholesterol is needed for all propercellular function.

High-density lipoprotein cholesterol (HDL-C),good cholesterol, helps reduce the risk of atherosclerosis bytaking cholesterol away from cells. Low density lipoprotein(LDL-C), bad cholesterol, carries cholesterol to cells. However, anLDL overload in the body increases a person's risk ofcardiovascular disease including atherosclerosis. "Our experimental findings indicate that statins, in addition tolowering LDL cholesterol, have clinical benefits of acceleratingplaque regression by a newly discovered mechanism," said co-authorMichael Garabedian, PhD, Professor, Department of Microbiology andUrology at NYU Langone Medical Center.

"It's possible that thesedrugs could possibly be more beneficial to a wider population ofpatients potentially reducing the overall lifetime burden of plaqueand the prevention of atherosclerosis." The study was a collaboration by NYU Langone Medical Center'sDepartment of Medicine, Division of Cardiology, the Department ofMicrobiology, Schneider Children's Medical Center of Israel and theCentre for Clinical Pharmacology, Division of Medicine at theUniversity College of London in the United Kingdom. This researchstudy was supported by funding from the National Institutes ofHealth, Astra Zeneca and Pfizer. Additional References Citations.

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