A key molecular switch that regulates heart cell division and normally turns the process off around the time of birth has been identified.
The findings could advance efforts to turn the process on and regenerate tissues damaged by heart attacks or disease.
"The children who helped us recognise the importance of this gene were born with a rare condition that leads to heart failure and many other problems, such as diabetes, obesity, blindness and deafness," said cardiologist Daniel P. Judge, director of the Johns Hopkins' heart and vascular institute's centre for inherited heart diseases.
Now we hope to apply these discoveries to help millions of others with heart disease, he added.
Things usually heal up well in many parts of the body through cell division, except in the heart and the brain.
This research offers an entirely different direction to pursue in finding ways to repair a damaged heart.
Unlike most other cells in the body that regularly die off and regenerate, heart cells rarely divide after birth.
When those cells are damaged by heart attack, infection or other means, the injury is irreparable.
The new findings emerged from insights into a genetic mutation that appears responsible for allowing cells to continue replicating in the heart in very rare cases.
The researchers hunted for genetic abnormalities that might account for the phenomenon by scanning the small percent of their entire genome responsible for coding proteins.
In experiments on mice, Johns Hopkins researchers found that the animals with the mutation had increased proliferation of heart cells after two weeks of age.
The cell proliferation did eventually stop in the mice.
"The mutation should advance the search for ways to help regenerate heart muscle tissue in a controlled fashion," Daniel P. Judge said.
