Hearts could learn to heal themselves
For decades cardiologists have had to accept that a damaged heart stays damaged. Once a heart attack kills off muscle cells they are gone for good, replaced by scar tissue that weakens the organ and often leads to heart failure.
That may be about to change, thanks to a team of scientists who have found a way of coaxing the heart to heal itself.
By reawakening a dormant gene known as CCNA2, which produces a protein called cyclin A2, researchers at Mount Sinai Hospital in New York made adult human heart cells divide and multiply in a laboratory — something long thought impossible. The results, published in the Nature Regenerative Medicine journal, suggest it may one day be possible to regrow heart tissue after injury, reducing the need for transplants or implanted pumps.
In Britain, more than 100,000 people are admitted to hospital each year after a heart attack, which equates to roughly one every five minutes.
A heart attack occurs when blood flow to part of the heart is blocked, starving it of oxygen and causing muscle tissue to die. About one million people in the UK live with heart failure, a chronic condition in which the heart becomes too weak to pump blood efficiently, often as a result of damage done by a heart attack.
In the womb, CCNA2 drives the growth of the developing heart — but the gene switches off soon after birth. Hina Chaudhry, the director of cardiovascular regenerative medicine at Mount Sinai’s Icahn School of Medicine, has spent nearly 20 years trying to reverse that process.
In 2014, her team became the first to regenerate a large mammal’s heart by reactivating CCNA2. They used pigs, whose hearts closely resemble those of humans, but now her group has produced evidence suggesting that the same approach could work in adult human heart cells.
After using a harmless virus to deliver an active version of CCNA2 into heart muscle cells taken from donor organs aged 21, 41 and 55, they watched the gene take effect using microscopes.
The most striking results were seen in the two older hearts. After the gene therapy, these mature cells began to stir. Under the microscope, the researchers watched them round up, reorganise, and then split in two.
When heart cells divide in the lab, they can lose their rhythm or shape, which would make them useless, or dangerous. In this study, the new cells retained the structure and proteins that give heart muscle its strength.
The next step will be to seek approval from America’s Food and Drug Administration to test the therapy in people with heart disease. “This is the culmination of nearly two decades of work,” Chaudhry said. “Now we’ve brought that vision one step closer to patients.”
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