Scientists have shown that cells in the heart's outer layer can migrate deeper into a failing organ to carry out essential repairs.
The key cells are shown in red
The migration of progenitor cells is controlled by a protein called thymosin beta 4, already known to help reduce muscle cell loss after a heart attack.
The discovery opens up the possibility of using the protein to develop more effective treatments for heart disease.
The University College London (UCL) study appears in the journal Nature.
Progenitor cells are similar to stem cells, in that they have the potential to turn into different types of adult tissue.
However, it had been thought there was no ready source of these cells in the heart, and to carry out repairs they had to be summoned up from the bone marrow.
The latest research is the first to show that they actually reside within the heart tissue itself.
The UCL team discovered that under the influence of thymosin ß4, progenitor cells in the outermost layer of the heart can be stimulated to form new blood vessels.
The researchers bred mice lacking thymosin ß4 in their hearts.
They found the hearts of these mice did not develop normally, the heart muscle showed early signs of tissue loss and blood vessel development was poor.
Closer examination revealed that without thymosin ß4, the progenitor cells failed to move deeper into the heart and change into the cells needed to build healthy blood vessels and sustain muscle tissue.
To investigate whether the protein could also help mend damaged adult hearts, the researchers took cells from the outer layer of adult mouse hearts and grew them in the lab.
Lead researcher Dr Paul Riley said: "We found that, when treated with thymosin ß4, these adult cells have as much potential as embryonic cells to create healthy heart tissue."
Dr Riley said using thymosin ß4 could lead to a more effective way to repair damaged hearts.
He said: "Our research has shown that blood vessel regeneration is still possible in the adult heart.
"In the future if we can figure out how to direct the progenitor cells using thymosin ß4, there could be potential for therapy based on the patients' own heart cells.
"This approach would bypass the risk of immune system rejection, a major problem with the use of stem cell transplants from another source.
"And, it has the added benefit that the cells are already located in the right place - within the heart itself."
The study was funded by the British Heart Foundation (BHF) and the Medical Research Council (MRC).
Professor Jeremy Pearson, BHF associate medical director, 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, a goal that researchers are urgently aiming for."
Professor Colin Blakemore, MRC chief executive, 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."