Dying of a broken heart is more common than you could think.
In fact, heart attack is the main health problem in people over 65, affecting just in US about 5 million persons and 1 in 5 Americans dies of heart attack. The problem comes from the fact that heart cannot regenerate after birth: its cells lose reproductive ability.
The damages produced by a heart attack cannot be fixed by new cells and the heart turns less efficient when pumping blood.
Now a team at the Columbia University Medical Center in New York has found a way to turn on a gene in adult mice that fixed their hearts after a heart attack, a research that could lead to techniques of fixing heart damage in human patients, excluding the need for a heart transplant.
The researchers manipulated a gene linked to cell reproduction and growth, enabling this way the adult mice to produce new cells replacing those dead after the heart attack.
"Heart cells don't divide at all in the mammal heart, and that's why we have so much mortality and morbidity," said co-author Dr. Hina Chaudhry.
Her team focused on the gene cyclin A2, which is very active in embryos, but turned off in adult mammals.
"We genetically engineered these mice to keep expressing this gene that becomes silent after birth," she said.
After that, the researcher induced a heart attack in the adult mice.They analyzed the mice after three months and discovered that the mice with engineered cyclin A2 genes displayed a 77 % better heart activity than the control mice.
"The mice who did not carry the gene were progressing to heart failure and dying. 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.
The team is planning now to test the method in larger mammals, a step towards applying the technique in treating human heart attack patients.
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