Scientists show heart can repair itself, with help

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LONDON (Reuters) – British scientists have managed to transform a type of stem-like cell in adult mouse hearts into functioning heart muscle in research proving that the heart has dormant repair cells that can be reactivated.

Although the research has yet to be translated into humans and is in its very 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 journal 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.


“These cardiomycytes can link into the existing muscle of the heart and they home to the area of injury,” Riley told reporters at a briefing in London. “And they are also both structurally and functionally coupled to the heart, and therefore represent a bona fide source of new heart muscle.”


He said that in this study the priming and boosting technique was able to improve the function of the damaged mouse hearts by up to 25 percent — an improvement which would make a dramatic difference to patients with heart failure if it could be translated into humans.


In previous studies, thymosin beta 4 has been shown to encourage regrowth of blood vessels and improve heart function after injury in mice, but this is the first time researchers have used it to regenerate functioning heart muscle.


Riley said his team was looking closely at this chemical and would be screening thousands of other potential drug candidates to see if they might have a similar effect on EPDCs.



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