When heart cells die – for instance after a heart attack – they cannot be replaced, as heart muscle cells are not normally able to divide to generate new tissue. In a new study published in Nature Communications, scientists attempting to study how overactivation of the gene Myc leads to cancer describe how they instead succeeded in activating heart muscle cells to divide, generating new heart tissue.
'This is really exciting because scientists have been trying to make heart cells proliferate for a long time. None of the current heart disease treatments are able to reverse degeneration of the heart tissue - they only slow progression of the disease. Now we've found a way to do it in a mouse,' said the lead author on the study, Dr Catherine Wilson from the University of Cambridge.
The Myc gene is normally active in dividing cells and switched off in non-dividing adult tissues, but gets reactivated in more than 50 percent of cancers, allowing tumour cells to divide and spread.
In the study, the researchers tried to understand Myc's role in cancer development, by overactivating it in different mouse tissues. They observed that although Myc activation led to new cell divisions in many tissues, heart cells remained dormant. Investigating why heart cells were resistant to Myc overactivation, the researchers found that when a second gene, called Cyclin T1, was also overactivated in heart cells, they were then able to divide.
The researchers hope that their findings will eventually be used to develop therapies for heart regeneration, but explain that this would have to be developed cautiously because Myc is a known oncogene.
'We want to use short-term, switchable technologies to turn on Myc and Cyclin T1 in the heart. That way we won't leave any genetic footprint that might inadvertently lead to cancer formation,' said Dr Wilson.