The heart can repair itself, new basic science suggests

Fascinating idea except for needing this in advance of your heart attack.
http://www.theheart.org/article/1236347.do?utm_campaign=newsletter&utm_medium=email&utm_source=20110609_EN_Heartwire

London, UK - British scientists have reported studies suggesting that it may be possible for the heart to repair itself after injury, and they have discovered a protein molecule that seems to stimulate this process [1].

Speaking at a press conference yesterday, Dr Peter Weissberg, medical director of the British Heart Foundation, which funded the research, 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. 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."
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He added: "Stem cells have been in the news for a while now, and there has been a lot of hype but perhaps not a lot of delivery, and we believe this is because the basic science has not been done properly. What we are publishing today is an example of really good basic science, which I believe will deliver the results we require."

Epicardial cells become cardiomyocytes

The research is published online June 8, 2011 in Nature. Senior author Dr Paul Riley (University College London, UK) explained that his team decided to investigate progenitor cells from the epicardium, as it is these cells in the embryo that become cardiomyocytes. "During pregnancy, these cells contribute to heart muscle and coronary blood vessels. 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."

In the paper, the researchers report that they restored the embryonic potential of these cells in mice by treating them with a peptide molecule called thymosin 4 (T4). The researchers primed adult mice with this peptide, and then, when damage to the heart occurred, a booster dose of T4 was given. They tracked the cells using a gene producing a green fluorescent protein and showed that after treatment with T4, the epicardial progenitor cells transformed into new cardiomyocytes and integrated with existing healthy muscle.

Riley said: "After treatment, the cells home to the site of injury and can couple and contract in the same way as normal cardiac myocytes, so structurally and functionally they represent a bone fide source of new heart-muscle cells." He added that mice treated in this way showed a 25% improvement in ejection fraction and reduced myocardial scarring and remodeling. The researchers are now testing T4 in human cells to see if they can replicate these results.

Weissberg commented: "If we could achieve a 25% 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."

Treatment required before MI occurs

Riley emphasized, however, that the formation of new myocytes and the resulting beneficial effects were not seen unless the mice were primed with T4 before heart injury. "We need to be able to treat in a preemptive way. So 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."

Weissberg added: "The target population would be patients who had had an episode of unstable angina. These patients are on the brink of having an MI. They are right on the edge of the precipice. There are millions of patients in this condition, and we treat them with drugs, but still many go over the precipice." He said it was not known whether the treatment would work on patients who had already had an MI but said as MIs evolved over several hours, it may be possible that it could be beneficial if given early after symptom onset.

Riley noted that T4 is already being developed as a medical treatment for skin conditions, but the researchers are aiming to find similar molecules that may be more efficacious at priming the epicardial cells. "While T4 has given us an insight into the potential of these cells, its efficacy is actually quite low. We are now testing libraries of substances that might be able to do a better job in this regard."

Weissberg added: "This is the classic drug-discovery approach. First, you find a molecular pathway that seems to have some benefit but isn't sufficiently active to give real clinical benefit. So then huge libraries of compounds are screened to find one that gives a better output. We are at the very beginning of that story."