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Scientists Discover Drug To Help Heart Repair Itself

June 9, 2011

A type of stem-like cell has been able to transform adult mouse hearts into functioning heart muscles that are able to repair itself, according to a study published in the journal Nature.

Although major advancements in heart disease prevention have reduced the number of people who die from heart attacks, the number of those living with heart failure are on the rise, with more than 750,000 people having the condition in the U.K. alone, reports BBC News.

The damage a heart attack causes when heart cells die as they become deprived of oxygen is currently permanent. As more and more dead tissue forms, heart failure can develop in patients where the heart can no longer be capable of pumping enough blood around the body.

Science investigations of how to regenerate heart tissue are being performed worldwide, but people with severe heart failure must live with mechanical devices, or hope for a heart transplant, for now.

The current study has yet to be translated into humans, since it is in the very early stages of development. However, the results give hope for the future.

“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,” says lead scientist Paul Riley of the University College London.

Professor Riley’s team focused their research on particular cells that are found in the outer layer of the heart called the epicardium-derived progenitor cells (EPDCs).

These cells are able to transform themselves into several specialist cells, including heart muscle, in developing embryos.

Previously, the EPDCs transforming ability was believed to be lost in adulthood, however, the study found that the molecule Thymosin beta -4, if used before the onset of a heart attack, can “prime” the heart to repair itself after damage.

In addition to causing heart attacks in the primed mice, the scientists also gave them a booster dose of theymosin beta-4, which prompted the EPDCs’ transformation into cardiomycytes, allowing them to 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. “And they are also both structurally and functionally coupled to the heart, and therefore represent a bona fide source of new heart muscle.”

According to the results, the priming and boosting technique was able to improve the function of the damaged mouse hearts by about 25 percent. If successfully translated to humans, it would make a dramatic difference to patients with heart failure.

Previous studies have shown that thymosin beta-4 encouraged regrowth of blood vessels and improved heart function after injury in mice; however, this is the first study to show that the molecule can help regenerate functioning heart muscle.

Further investigations into the effects of thymosin beta-4 are needed, according to Riley. In addition, his team will be screening other potential drug candidates for possible similar effect on EPDCs.

Riley says that a drug could be available to humans in about 10 years.

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