Most body tissues can repair themselves, with the help of nearby dividing cells. Cuts on the skin, for example, heal easily within a couple of days. But cells in the heart lose the ability to divide soon after birth. This means that the death of heart cells, brought on by a heart attack or other conditions, can lead to heart failure, where the heart can no longer pump enough blood around the body.
Now, scientists are one step closer to understanding why this happens. An international team led by Dr Hesham Sadek of the University of Texas, US, found that the expression of a gene called Meis1 increased in mice after they were born. Levels of Meis1 increased steadily for seven days after birth, after which the heart became unable to self-heal.
When they disabled the gene, heart cells kept on dividing in the mice well into adulthood, and their hearts were found to contain more cells than control mice with the intact gene. However, when Meis1 was overexpressed in newborn mice, their hearts failed to heal after being damaged.
'Meis1 is a transcription factor, which acts like a software program that has the ability to control the function of other genes', explained Dr Sadek. 'In this case, we found that Meis1 controls several genes that normally act as brakes on cell division'.
The findings provide a better understanding of the genes controlling heart development, and hint at a possible gene therapy approach to treating human heart failure. 'Meis1 could possibly be used as an on/off switch for making adult heart cells divide. If done successfully, this ability could introduce a new era in treatment for heart failure', says Dr Sadek.
But any new treatment for human heart conditions is likely to be a long way off, as the study only featured mice. Professor Jeremy Pearson, associate medical director at the British Heart Foundation, told the Telegraph: 'This [research] opens up the exciting prospect that blocking Meis1 will encourage heart muscle to regenerate and repair heart function after a heart attack. Further research is now needed to confirm this, and to design ways of blocking Meis1 that could be used clinically'.
The study was published last week in the journal Nature.