Researchers have discovered a molecule that could play a role in treating and preventing heart failure.
The molecule provides the heart with a tool to block a protein that interferes in normal genetic activity when the heart is subjected to stress, leading to heart failure.
By restoring levels of the molecule in mice experiencing heart failure, the progression of the failure was stopped.
The molecule is a non-coding RNA, which the team named Myheart — myosin heavy-chain-associated RNA transcript — controls a protein called BRG1.
In its earlier work, the team had seen that the protein which is crucial for the development of the heart in the foetus turns into a disruptor at later stages, especially when the heart undergoes stress as that from high blood pressure.
During such periods of stress, it was noticed that production of Myheart is suppressed, leading to uncontrolled hara-kiri by BRG1.
In the current Nature paper, the researchers reported that in mice with stress-induced high levels of BRG1, they were able to restore Myheart to normal levels using gene transfer technology and in the process prevent heart failure.
"I think of Myheart as a molecular crowbar that pries BRG1 off the genomic DNA and prevents it from manipulating genetic activity," said team leader Dr Ching-Pin Chang, director of molecular and translational medicine, at the Krannert Institute of Cardiology.
Before testing the molecule in humans, the team is trying to identify smaller areas of Myheart involved in the blocking activity. This is because Myheart is too big a molecule to be delivered as a drug.
A subsection of the Myheart molecule could lead to a compound to test in human trials.