Suppressing Gene Prevents Heart From Aging And Improves Cardiac Function

by Aruna on  October 15, 2009 at 10:45 AM Research News   - G J E 4
Suppressing Gene Prevents Heart From Aging And Improves Cardiac Function
A new study has found that suppressing a form of PI3K gene successfully prevented heart from aging and preserved its function in mice.

The findings of the study could help physicians to one day prevent age-related heart failure in humans.

"The study provides evidence that delaying or preventing heart failure in humans may be possible," said Dr. Tetsuo Shioi, senior author of the study and assistant professor of medicine at Kyoto University Graduate School of Medicine in Kyoto, Japan.

"Advanced age is a major risk factor for heart failure. One reason is that aging increases the chance of exposure to cardiovascular risk factors. However, natural changes due to aging may also compromise the cardiovascular system," added Shioi.

The researchers studied elderly mice genetically engineered to suppress the activity of one form of the PI3K gene, which is a part of the insulin/IGF-1 signaling system that helps regulate the lifespan of cells.

A variation of PI3K, known as the p110a isoform, plays an important role in tissue aging.

Suppressing the isoform's activity in the roundworm C. elegans extends its life.

And in fruit flies, suppression prevents the age-dependent decline of heart function.

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 researchers concluded that PI3K's role in cardiac aging involved regulating other points further downstream in the insulin/IGF-1 signaling pathway, which resulted in changes in how insulin acted in heart cells.

The biological mechanism by which suppressing the gene's activity improved the survival of the mice remains unclear.

The study was published in Circulation: Journal of the American Heart Association.

Source: ANI

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