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,