CHICAGO (Reuters) - Researchers have figured out how to switch on a gene in adult mice that repaired their hearts after a heart attack, a finding that may one day help fix heart damage in humans.
The team at Columbia University Medical Center in New York found that by genetically manipulating a gene associated with cell growth, adult mice were able to make new cells to replace those damaged in a heart attack.
Heart cells in mice, and in humans, stop regenerating after birth. If the heart is damaged by a heart attack, it cannot create new cells to repair the damage and hearts become less efficient at pumping blood.
“Heart cells don’t divide at all in the mammal heart, and that’s why we have so much mortality and morbidity,” said Dr. Hina Chaudhry, whose study appears in the journal Circulation Research.
Chaudhry and colleagues studied the gene cyclin A2, a gene that is active in embryos, but shut off in adult mammals.
“We genetically engineered these mice to keep expressing this gene that becomes silent after birth,” she said in a telephone interview.
The researchers then induced a heart attack in the mice.
At three months, the mice whose cyclin A2 genes had been switched on had 77 percent better heart function than the other mice.
“The mice who did not carry the gene were progressing to heart failure and dying,” she said. “We didn’t lose any of the mice that carried the gene. They had much better survival.”
“We’re the first study to show a sustained improvement in cardiac function by any kind of molecular or cellular manipulation,” she said.
Heart failure is the leading cause of hospitalization in people older than 65, a condition that affects nearly 5 million Americans.
Chaudhry said the approach needed to be tested in larger mammals and then in humans, something she believes is not too far off.
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