Tweaking DNA and two weeks exercise equivalent in healing heart

According to the researchers, altering the DNA sequence is equivalent to a fortnight long exercising routine, in working against a heart injury.

The study was spearheaded by Dr. Bruce Spiegelman, Professor of Cell Biology at Harvard Medical School's Dana-Farber Cancer Institute, and his contemporaries, who aimed to derive a gene switch that could help in counteracting a heart injury.

Lead author, Dr. Bruce Spiegelman said, "If we learned to manipulate this pathway with specific exercise regimens or with drugs, we might be able to achieve some of the benefits produced by exercise-related heart enlargement."

“It's well documented that exercise has beneficial effects on metabolism and skeletal muscle, but we hypothesized that it might also have more direct beneficial effects in the heart itself that could be exploited to protect against heart failure,” added co-author Dr. Anthony Rosenzweig, who is a cardiologist at the Harvard's Beth Israel Deaconess Medical Center.

Study details
The preliminary trials for the present study were conducted on mice and the positive results urged the investigators to launch further intensive research and develop a genetic cure for repairing an injured human heart.

According to the researchers, “The genetic manipulation of the gene C/EPB-beta – spurred the animals' heart muscle cells – called cardiomyocytes – to proliferate and grow larger by an amount comparable to normal mice that swam for up to three hours a day.”

Also, they said that the mice had slightly enlarged hearts that showed defiance to cardiac stress just like in the valvular heart disease or the effects of high blood pressure.

This observation led the study authors in believing that a treatment could be derived for the heart, through genes.

Important finding
The study points out at an alternative healing method for the human heart that could help people facing difficulty doing the endurance exercises, post a heart injury.

“The more robust cardiomyocytes are likely to have played an important role in the resistance to heart failure. By understanding the pathways that benefit the heart with exercise, we may be able to exploit those for patients who aren't able to exercise,” informed the lead investigator.

He concluded, “If there were a way to modulate the same pathway in a beneficial way, it would open up new avenues for treatment.”

The findings of the research are published in the December issue of the journal 'Cell.'