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Study reveals potential new target for cholesterol-lowering drugs

DALLAS March 29, 2005 Mice lacking a key protein involved in cholesterol regulation have low-density lipoprotein, or "bad" cholesterol, levels more than 50 percent lower than normal mice, and researchers suggest that inhibiting the same protein in humans could lead to new cholesterol-lowering drugs.

In a study to be published in the Proceedings of the National Academy of Sciences and available online this week, researchers at UT Southwestern Medical Center deleted the Pcsk9 gene in mice. The gene, present in both mice and humans, makes the PCSK9 protein, which normally gets rid of receptors that latch onto LDL cholesterol in the liver. Without this degrading protein, the mice had more LDL receptors and were thus able to take up more LDL cholesterol from their blood.

"The expression of LDL receptors is the primary mechanism by which humans lower LDL cholesterol in the blood," said Dr. Jay Horton, associate professor of internal medicine and molecular genetics and senior author of the study. "This research shows that in mice, deleting the PCSK9 protein results in an increase in LDL receptors and a significant lowering of LDL cholesterol."

High LDL cholesterol is a major risk factor for heart disease, heart attack and stroke because it contributes to the buildup of plaque that clogs the walls of arteries. Nearly 25 million people worldwide take a class of drugs called statins to lower their cholesterol to within recommended healthy levels.

On average, mice lacking the Pcsk9 gene, called knockout mice, had blood LDL cholesterol levels of 46 milligrams per deciliter, while wild-type mice had levels around 96 mg/dl, a difference of 52 percent.

Dr. Horton's research is consistent with findings from another recent UT Southwestern study showing that humans with mutations in their PCSK9 gene, which prevented them from making normal levels of PCSK9 protein, had LDL cholesterol levels 40 percent lower than individuals without the mutation
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Contact: Amanda Siegfried
amanda.siegfried@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
29-Mar-2005


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