By Nick Carne
The quest to find a curative treatment for heart disease may have taken an unexpected turn.
Researchers from the University of Cambridge, UK, report that in studies with mice they found a gene that promotes cancer in other parts of the body but appears to trigger regeneration in the heart.
That’s significant because adult hearts cannot usually repair themselves once damaged, and current treatment options cannot reverse the degeneration, only slow it down.
It may also explain why heart cancer is extremely rare, notes Catherine Wilson, lead author of a paper in the journal Nature Communications.
“This is really exciting because scientists have been trying to make heart cells proliferate for a long time,” she says.
Cancer develops when cells start to replicate uncontrollably. The Myc gene plays a key role in this process and a great deal of research has focused on trying to control Myc as a means of cancer therapy.
When Wilson and colleagues made Myc overactive in a mouse model, they saw its cancerous effects in organs, including the liver and lungs: huge amounts of cells started replicating over the course of a few days. But in the heart, nothing much happened.
They found that Myc-driven activity in heart muscle cells is dependent on the level of another protein called Cyclin T1, made by a gene called Ccnt1, within the cells.
When the Ccnt1 and Myc genes are expressed together, the heart switches into a regenerative state and its cells start to replicate.
“When these two genes were overexpressed together in the heart muscle cells of adult mice, we saw extensive cell replication, leading to a large increase in the number of heart muscle cells,” says Wilson.
After a heart attack, an adult human heart can lose up to one billion heart cells, which are never replaced. Their loss reduces the strength of the heart and causes scar formation, heart failure and ultimately death.
The researchers say they hope to a genetic therapy for the treatment of heart disease.
“We want to use short-term, switchable technologies to turn on Myc and Cyclin T1 in the heart. That way we won’t leave any genetic footprint that might inadvertently lead to cancer formation,” says Wilson.