Revealed: how damaged hearts may learn to heal themselves

Millions of people suffering from heart disease have been given new hope by research which shows that damaged organs may be capable of healing themselves.

A team of scientists at the Institute of Child Health in London have discovered that cells in the outermost layer of the heart can be stimulated to move deeper inside the heart muscle and, once there, help to repair a failing organ.

They say that their discovery is a "major step" towards developing a DIY repair mechanism for heart disease, which kills more than 105,000 people every year in the UK.

The first picture illustrating the discovery, entitled "Cells to repair a broken heart", was a winner in the annual British Heart Foundation Science Image competition, whose results were announced yesterday.

The discovery could lead to injections being given into the bloodstream or, in emergency cases, directly into the heart muscle itself. So far the technique has only been tested on rats and mice but, if it is proved to work in humans, it could be developed into a treatment in "years rather than decades", according to Paul Riley, who led the study.

Dr Riley, of the ICH, said: "Our research has shown that blood vessel regeneration is possible in the adult heart. In the future ... there could be potential for therapy based on the patients' own heart cells."

Treating a damaged heart following a heart attack is difficult because a section of heart muscle dies and the tissue has a limited ability to respond. The team have found that cells in the outer layer of the heart are similar to stem cells, and have the capacity to develop into any kind of new tissue or structure in the heart. Called progenitor cells, they can be stimulated by a protein, Thymosin-beta4, to move into the heart muscle and form new blood vessels. With new blood vessels to carry oxygen and nutrients, the damaged heart muscle can grow new tissue and repair itself.

It had been thought that cells of the adult heart were in a state of permanent rest and that any progenitor cells involved in repair of heart muscle had to migrate into the heart from the bone marrow. But, Dr Riley said: "The progenitor cells are already located in the right place - within the heart itself. All that these cells need is the appropriate instructions to guide them towards new blood vessel formation that will help in the repair of muscle damage following a heart attack.''

The research was carried out on mice bred to lack Thymosin-beta4 in their hearts. The team found that the hearts of these mice did not develop normally, with the heart muscle showing early signs of tissue loss, and blood vessel development being poor.

Dr Riley said: "To investigate whether Thymosin-beta4 could have a therapeutic effect on damaged adult hearts, my research team took cells from the outermost layer of adult mouse hearts and grew them in the lab. We found that, when treated with Thymosin-beta4, these adult cells have as much potential as embryonic cells to create healthy heart tissue. This suggests that Thymosin-beta4 could have a therapeutic use."

Experiments on animals have shown that by infusing stem cells from bone marrow into the heart after a heart attack, the organ can be helped to grow strong again. Stem cell transplants have been seen as a potential treatment for heart failure following heart attack. But, as with all transplants, an immune response kicks in and rejection of the transplanted material is possible.

The advantage of Dr Riley's research, funded by the British Heart Foundation (BHF) and the Medical Research Council and published in the journal Nature in November, is that it demonstrates that the healing stem cells are already present in the heart, thereby eliminating the need for a transplant.

Professor Jeremy Pearson, associate medical director at the BHF, said: "These results are important and exciting. By identifying for the first time a molecule that can cause cells in the adult heart to form new blood vessels, Dr Riley's group have taken a large step towards practical therapy to encourage damaged hearts to repair themselves. That is a goal that researchers are urgently aiming for."

The chief executive of the Medical Research Council, Professor Colin Blakemore, said: ''Finding out how this protein helps to heal the heart offers enormous potential in fighting heart disease, which kills more than 105,000 people in the UK every year.

"This is an excellent example of the way in which first-class research, at the most basic molecular level, can produce opportunities for translation into innovative new treatments that should help patients and improve their lives."

Curse of the Western lifestyle

In Britain, some 300,000 people suffer a heart attack each year, a third of whom die. The death rate is among the highest in western Europe.

The heart is a muscle that pumps 100,000 times a day to carry oxygen and nourishment to the furthest extremities of the body.

It is vital to sustaining life but prey to the excesses of a Western lifestyle - little exercise, fatty diets and smoking.

The effects of that lifestyle - the early signs of heart disease - can be seen even in children and are universally present in adults. Heart disease is caused by a build-up of fatty deposits, or atheroma, that narrow the arteries and increase the risk of a blockage caused by a blood clot.

Coronary heart disease is so-called because it affects the "crown" or corona of tiny arteries that sits on top of the heart and provides oxygenated blood to the heart muscle to keep it pumping. These small arteries are especially prone to narrowing and to blockage by a clot or thrombus of blood. When that happens it triggers a coronary thrombosis, or heart attack.

Smoking increases the stickiness of the blood and its propensity to form clots, while cholesterol plays a key role in generating the fatty deposits that leads to atheroma.