Dr. Jorg-Detlef Drenckhahn, a researcher from the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch, said that it was while experimenting with female mice that the team observed that the healthy cells of the heart divide more frequently and displace the damaged tissue.
"Hopefully, our results will lead to new therapies in the future. With the right signals, a heart that has been damaged - for example through infarction - might be stimulated to heal itself," Dr. Drenckhahn said.
During the study, the researchers switched off a gene called Holocytochrome C synthase (Hccs) in the developing hearts of mice.
Since Hccs is essential for energy production, the defective energy production due to the switching off of the gene caused the embryos to die.
However, the animals that still had some healthy myocardial cells survived, and at the time of birth they had a heart that was fully able to function.
The researchers also observed that up until birth, the foetal heart managed to improve the ratio of healthy cells to defective cells from the original 50:50 ratio.
The defective cells then only comprised 10 per cent of the entire heart volume, possible because the healthy myocardial cells divide much more frequently than the defective cells.
The team said that the percentage of healthy cells in the heart increases so that, at the time of birth, the ratio is large enough to allow the heart of the newborn mouse to beat normally.
"But even for a while after birth, the heart is capable of compensatory growth of healthy cardiac cells," Dr. Drenckhahn said.
The heart later loses this ability, according to the researchers, because of which some of the mice died of myocardial insufficiency after about one year, and almost half developed arrhythmia.
The team has yet to discover why only some of the mice developed heart problems, and thus they want to inactivate the gene in adult mice as well in order to investigate its influence.
They also want to identify the foetal signal substances that stimulate healthy cells to proliferate and inhibit diseased cells, something that they believe may help stimulate the body's own repair mechanisms of the heart an attack or in the case of heart insufficiency.
An article on the research has been published in the journal Developmental Cell.