U.K. study shows potential for heart to repair itself

A study headed by Paul Riley and a team from University College London showed that dormant repair cells in the hearts of adult mice can be reactivated by transforming dormant cells from the epicardium with the injection of thymosin beta 4, according to Reuters.

It has yet to be seen whether similar results can be elicited in human hearts, and the research is still in a very early stage. However, it does indicate that there is the possibility that a drug could be developed that can prompt hearts that have undergone cardiac arrest into self repair, Reuters said.

The research was funded by the British Heart Foundation. Dr. Peter Weissberg, medical director said, “We have always believed that the heart has no capacity to heal itself, but this research suggests that this is not the case. We think we have discovered a natural process that brings about repair of the heart,” according to theheart.org.

Weissberg said in a press conference, “Until now, this has been science fiction. We are trying to understand what the triggers are for this process. The cells that are capable of this healing are already there in the epicardium. They just need to be tweaked and primed and the effect scaled up. If this works, we might be able to heal cardiac injury caused by heart attacks without resorting to stem cells,” theheart.org reported.

Riley, who heads the research team, told Reuters, “I could envisage a patient known to be at risk of a heart attack taking an oral tablet…which would prime their heart so that if they had a heart attack the damage could be repaired.”

Regeneration of heart tissue

In recent years, the number of deaths caused by heart attacks has gone down with medical advances. What has yet to be addressed is debilitation caused by the incidence of heart failure leading to a specific accumulation of dead heart tissue, Reuters reported.

Presently, mechanical devices are used in such case, or a transplant. But Riley’s study, which came out in the June 8, 2011, online publication Nature, targeted progenitor cells from the epicardium, or outer layer in the heart, Reuters said.

Riley said he targeted these progenitor cells because in an embryo, they become cardiomyocytes. “During pregnancy, these cells contribute to heart muscle and coronary blood vessels,” theheart.org reported.

Riley added, “In the adult, these cells sit in a dormant state. We think there is a possibility that these cells might be able to be activated to switch on the embryonic gene that causes them to make new myocardial cells,” according to theheart.org.

Thymosin beta 4

Riley found out that by injecting the healthy hearts of adult mice with thymosin beta 4, they can be “primed” to repair themselves after damage, according to Reuters.

After injecting the healthy hearts of the adult mice with thymosin beta 4, the researchers initiated heart attacks in the mice. They then gave the same mice another booster dose of thymosin beta 4. This prompted the transformation of dormant progenitor cells into cardiomycytes, Reuters said.

Riley said, “These cardiomycytes can link into the existing muscle of the heart and they home to the area of injury. [T]hey are also both structurally and functionally coupled to the heart, and therefore represent a bona fide source of new heart muscle,” Reuters reported.

The mice who received the treatment experienced a 25 percent improvement in the heart’s ejection fraction. There was also a reduction of myocardial scarring and remodeling, theheart.org said.

Preemptive treatment

Attempts are being made to see if the treatment will be effective on human cells. However, Riley emphasized that the treatment is primarily preemptive. It must be applied before heart injury, according to theheart.org.

Riley said, “We would need to treat patients at high risk of having a heart attack before that heart attack occurred. That is the key. The idea would be to identify these high-risk individuals and then give them this medication that would keep them their cells in a primed state, so that if an MI occurs repair would occur,” according to theheart.org.

Weissberg said, “If we could achieve a 25 percent increase in ejection fraction in humans, that would be a substantial effect. However, we rarely see in [humans] the same benefit as is shown in animal studies. But even if we could achieve a 10% improvement, that would make a major difference to quality of life,” theheart.org reported.