Study: Preserving Heart Function Prevents Aging

Study: Preserving Heart Function Prevents Aging

Reported October 13, 2009

(Ivanhoe Newswire) — Scientists prevented age-related changes in the hearts of mice and preserved heart function by suppressing a form of the PI3K gene, according to a new study.

“The study provides evidence that delaying or preventing heart failure in humans may be possible,” Tetsuo Shioi, M.D., Ph.D., senior author of the study and assistant professor of medicine at Kyoto University Graduate School of Medicine in Kyoto, Japan, was quoted as saying.

According to the American Heart Association, 5.7 million Americans have heart failure, and nearly 10 out of every 1,000 people over age 65 suffer heart failure every year.

Shioi and his colleagues studied elderly mice genetically engineered to suppress the activity of one form of the PI3K gene, called the p110a isoform, which plays an important role in tissue aging. Suppressing this isoform has been shown to prevent the age-dependent decline of heart function in round worms and fruit flies.



The Japanese researchers compared aged mice with a functional p110a to aged mice with suppressed p110a and found that mice with the suppressed gene had improved cardiac function, less fibrosis (fibrosis causes the heart to lose flexibility), fewer biological markers of aging, and a pattern of cardiac gene expression like that of younger mice.

“This study showed that aging of the heart can be prevented by modifying the function of insulin and paves the way to preventing age-associated susceptibility to heart failure,” said Shioi.

“The heart failure epidemic in the United States and many other countries is due, in part, to our aging population,” Mariell Jessup, M.D., an American Heart Association spokesperson and professor of medicine at the University of Pennsylvania School of Medicine in Philadelphia, was quoted as saying. “Aging humans experience a slow but gradual loss of heart cells and a host of other cellular and sub-cellular abnormalities which make the remaining cells contract less efficiently. Thus, this early work in a mouse model, clarifying the role of PI3K in cardiac aging, could ultimately allow scientists to understand if human hearts are similarly influenced.”

SOURCE: Circulation: Journal of the American Heart Association, October 12, 2009