Potential Heart Disease Treatment Identified

By Emma Patten-Hitt, PhD

NEW YORK (Reuters Health) - Scientists have identified a protein that may contribute to heart disease by causing fat to be deposited in the walls of arteries. The protein, researchers suggest, may serve as a therapeutic target for the prevention of this fatty build-up, called atherosclerosis.

Atherosclerosis, the leading cause of death in most Western countries, can restrict the flow of blood through blood vessels. When left unchecked, this can raise the risk of a heart attack.

In their study, Dr. MacRae F. Linton from Vanderbilt University in Nashville, Tennessee, and colleagues used mice specially bred to develop extremely high blood cholesterol levels and atherosclerosis. They also made some of these mice deficient in a protein called aP2.

The investigators found that the mice lacking the aP2 protein were less likely to develop atherosclerosis than were mice that did have the protein, indicating the importance of the protein in the development of atherosclerosis.

The protein, according to Linton's team, contributes to the development of atherosclerosis, because it helps immune system cells called macrophages accumulate fat. Once filled with fat, the cells stick to the walls of arteries, causing the fatty build-up of atherosclerosis.

``Although there are no immediate therapeutic implications, these studies clearly define aP2 as a target for the development of therapies to prevent atherosclerosis,'' Linton told Reuters Health.

Linton also pointed out that mice deficient in the protein are more sensitive to the hormone insulin and have lower triglyceride levels, suggesting that therapies targeting this protein may be important for both diabetes and heart disease. Insulin helps regulate blood sugar levels, and insulin sensitivity is a key factor in developing diabetes, while high triglyceride levels help contribute to heart disease.

``Our findings have direct and very exciting therapeutic possibilities,'' study co-author Dr. Gokhan Hotamisligil, of Harvard University, Boston, Massachusetts, told Reuters Health.

``This is a brand new, previously unrecognized pathway controlling atherosclerosis,'' he said. ``This is both valuable scientific insight and provides new opportunities for prevention and treatment.''

SOURCE: Nature Medicine 2001;7:699-705.

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