Wake Forest Researchers Receive Renewed Funding to Study Cardiovascular Disease
WINSTON-SALEM, N.C. -- Wake Forest University School of Medicine researchers have received a $9 million grant from the National Heart, Lung and Blood Institute (NHLBI) to continue research in the development of hardening of the arteries—or atherosclerosis.
Earlier this year, it was reported in the Proceedings of the National Academy of Sciences that a research team from Wake Forest University Baptist Medical Center and the University of California, San Francisco, had determined that an enzyme found only in the liver and intestines might play a crucial role in the development of atherosclerosis.
That team was led by Lawrence L. Rudel, Ph.D., professor of pathology and biochemistry at Wake Forest, and he is the principal investigator of the renewed grant.
Confirmation of the relationship between the enzyme, ACAT2, and low-density lipoproteins (LDL)—the bad cholesterol in blood—may point to a new way of treating hardening of the arteries.
Coronary heart disease is the leading cause of death in the United States. The narrowing of arteries through atherosclerosis is a major contributor to heart attacks and strokes. New information defining the relationships between cholesterol and coronary heart disease comes from research such as is planned in this program.
The grant will be distributed over five years.
Project leaders in the grant at Wake Forest University include:
- John S. Parks, Ph.D., professor of pathology and associate professor of biochemistry and Mary G. Sorci-Thomas, Ph.D., also professor of pathology and associate professor of biochemistry, who will do studies designed to help understand the role of high-density lipoprotein (HDL)--good cholesterol--in the disease process.
- Gregory S. Shelness, Ph.D., associate professor of pathology and Paul A. Dawson, Ph.D., associate professor of internal medicine-gastroenterology and associate professor of comparative medicine who will investigate how LDL forms and how LDL promotes development of atherosclerosis.
Many of the studies will take advantage of genetically engineered mouse models in which the contribution of specific gene products can be ascertained.
The program project represents a continuation of a grant that has been funded for 10 years. Over that period, the research has led directly to more than 150 original peer-reviewed publications in scientific journals.
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