THURSDAY, Nov. 10, 2005 (HealthDay News) -- It's the job of specialized bone marrow cells to repair damage to the lining of arteries, and the failure of these cells to keep up with that deterioration may be key to atherosclerosis (hardening of the arteries), researchers report.
Researchers at Duke University also identified clusters of genes that are expressed at distinct phases of atherosclerosis progression.
"These results provide us with an intriguing new understanding of the disease process involved in atherosclerosis," cardiologist Dr. Pascal Goldschmidt, senior member of the research team and chairman of Duke's Department of Medicine, said in a prepared statement.
As reported early online and published in the Nov. 15 issue of the Proceedings of the National Academy of Sciences, the study is the first to link a deficiency in the body's repair mechanisms to the progression of any kind of chronic disease.
According to the Duke team, risk factors such as smoking, high cholesterol, inactivity, and poor diet are important in developing atherosclerosis. This study suggests that genetics also plays a major role in how a person responds to these risk factors.
"It appears that the disease progresses as the body's intrinsic ability to repair and rejuvenate itself somehow becomes defeated," Goldschmidt said. "It is exciting for us to think that if we as physicians could somehow stimulate or maintain a successful repair process in heart patients, we might be able to prevent the development of atherosclerosis even if we can't completely control other risk factors, such as high lipid levels or hypertension."
More information
The U.S. National Heart, Lung, and Blood Institute has more about atherosclerosis.
