Scientists have provided new details about how a drug used against heart disease helps to unclog blood vessels from an excess of cholesterol and fats. The results help explain how the drug works and may provide ways to improve similar drugs in the future.
A type of white blood cell called macrophage is responsible for the accumulation of fat in blood vessels, leading to inflammation and plaque formation on the inner linings of the vessel. Macrophages produce enzymes called lipases that have been shown to promote fat accumulation in blood vessels. Drugs called statins reduce the accumulation of fat in macrophages but their effects on lipases have not been explored yet.
John S. Hill and colleagues studied the effect of a statin drug called atorvastatin on two lipases, called lipoprotein lipase and endothelial lipase, which break down different types of fats. The researchers showed that the statin significantly reduced the levels of both lipases in macrophages and described in detail the proteins that are affected within the macrophages. These results may help to understand how other statin drugs work and could help design better drugs against heart disease in the future, the scientists conclude.
Article: "Atorvastatin Decreases Lipoprotein Lipase and Endothelial Lipase Expression in Human THP-1 Macrophages," by Guosong Qiu and John S. Hill
The above post is reprinted from materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.
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