Although the research has yet to be translated into humans and is in its early stages, the results suggest that in the future, a drug could be developed to prompt and prime hearts damaged by cardiac arrest into repairing themselves.
“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,” said Paul Riley of University College London, who led the study.
Major advances in medical science in recent years have helped cut the number of people who die from heart attacks, but the damage an attack causes — when heart cells die as they become starved of oxygen — is currently permanent.
If enough dead tissue forms, patients can develop heart failure, a debilitating condition in which the heart is not able to pump enough blood around the body. Scientists around the world are investigating various ways to regenerate heart tissue, but for now people with severe heart failure must use mechanical devices or hope for a transplant.
Riley’s team, whose study was published in the Nature Wednesday, targeted particular cells found in the outer layer of the heart, called the epicardium. These cells, referred to as epicardium-derived progenitor cells (EPDCs), are known to be able to transform into a number of specialist cells, including heart muscle, in developing embryos.
Scientists had previously thought EPDCs’ ability to transform was lost in adulthood, but in this study Riley’s team found that by treating the healthy hearts of adult mice with a molecule called thymosin beta 4, they were able to “prime” the heart to repair itself after damage.
After causing heart attacks in the primed mice, the researchers also gave them a booster dose of thymosin beta 4 and this prompted the EPDCs to transform into cardiomycytes, and integrate with existing muscle.
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