Mice is able to fix their own heart cells with a gene switch after an heart attack.
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.
Heart cells in humans as well as in mice stop regenerating after birth, so when the heart is damaged by a heart attack, the cells get damaged and no longer is able to produce newer cells to replace the damaged ones. As a result, the heart becomes weaker and less efficient at pumping blood. Scientists at Columbia Medical Center, New York, are trying to replace the gene that triggers new cell growth. They replaced the defective gene with a newer one in adult mice and were able to show new cell growth to replace those damaged ones in a 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 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 shuts off itself after birth in adult mammals.
Dr. Chaudhry wants to refine this gene via genetical engineering, so that it keeps on producing cells even after embryo stage.
They did a trial with the mice; they induced a heart attack in mice and observed it after three months. The mice whose cyclin A2 genes were switched on had 77% better heart functions than the other mice.
The mice which don’t carry this gene become worse with heart failure and dies. Whereas the mice that carry the cyclin A2 gene, survived longer.
"We're the first study to show a sustained improvement in cardiac function by any kind of molecular or cellular manipulation," she said.
Nearly 5 million Americans suffer from heart failure and is the leading cause of hospitalization in people older than 65.
Before this study is extended to humans, Dr. Chaudhry wants to test it on other mammals and eventually in humans. She firmly believes that this technique will be employed soon.