A team based at the UCL Institute of Child Health (Great Ormond Street Hospital’s research partner) have achieved a breakthrough in the treatment of heart disease, after finding a means of repairing cells damaged during cardiac arrest in mice.

The study – funded by the British Heart Foundation (BHF) – proves the heart has dormant repair cells in its outer layer that may be re-activated, suggesting that in the future hearts damaged by a heart attack could be encouraged to repair themselves.

The team, led by Professor Paul Riley, targeted cells called progenitor cells in the epicardium, the outer layer of the heart. In the embryo, these epicardium-derived progenitor cells (EPDCs) are able to transform into a number of specialist cells including heart muscle. Scientists thought this ability was lost in adults (damage caused by a heart attack is currently permanent) but the researchers have managed to reactivate this potential.

They restored the cells’ potential by treating the healthy hearts of adult mice with a protein called thymosin β4 (Tβ4). This appeared to ’prime’ the heart for repair. When damage to the heart occurred, a booster dose of Tβ4 was given, and this sparked the cells to transform into new heart muscle and integrate with existing healthy muscle. Crucially, muscle is not formed if the EPDCs have not been pre-treated with Tβ4.

Treatments based on this method are several years away, as Tβ4 enabled only a limited number of heart muscle cells to be generated. A pill that enables damaged hearts to repair themselves could be available within ten years, although researchers believe it would probably take the form of a preventative drug for people at high risk.

Paul Riley said: “This is an important piece of work and something we’ve been working toward for some time. Our earlier research proved blood vessels could be regenerated in adult hearts but there were major doubts about whether the same might be true for heart muscle. This work has demonstrated a possible method for repairing hearts damaged by a heart attack and could have a major impact on future therapies to treat heart failure.”