A cardiac molecule - called Myheart - could lead to new treatment and prevention strategies for heart failure.
Heart failure occurs when the heart is unable to pump enough blood and oxygen around the body to support other organs. It can be caused by a number of medical conditions, including high blood pressure (hypertension), heart disease and diabetes.
If heart failure is diagnosed early, there are medications - such as beta blockers and statins - that can help improve a patient's quality of life. Daily physical activity and a healthy diet may also help slow its progression.
But the researchers of this latest study - led by Dr. Ching-Pin Chang, associate professor of medicine at the Indiana University School of Medicine - say a new prevention and treatment strategy for heart failure could be in the cards with the discovery of a long non-coding RNA (ribonucleic acid), which they call Myheart (myosin heavy-chain-associated RNA transcript).
The researchers explain that RNA is normally responsible for carrying instructions, or a "code," from the DNA in a cell's nucleus to parts of the cell that create proteins crucial for cell activities.
Myheart stops protein from altering genetic material, preventing heart failure
Recent research has uncovered a number of long non-coding RNAs, which act on their own rather than carry instructions. The role these RNAs play in the heart has been a mystery.
But in this latest study, published in the journal Nature, Dr. Chang and colleagues found that the long non-coding RNA Myheart controls BRG1 - a protein that a 2010 study from the team found is crucial to heart development in the fetus.
In the previous study, the researchers found that only small amounts of BRG1 are produced as the heart matures. However, they found that when the heart is subject to stress - such as hypertension or damage from a heart attack - BRG1 production is increased. This interferes with genetic activity in the heart, causing heart failure.
The researchers explain that Myheart production is halted during this process, meaning BRG1 attaches to DNA and has free reign over alteration of genetic material.
In the new study, the researchers used gene transfer technology to restore Myheart to normal levels in mice that had high levels of BRG1. The researchers say this stopped BRG1 from altering the heart's genetic material and prevented heart failure in the mice.
Commenting on the discovery, Dr. Chang says:
"I think of Myheart as a molecular crowbar that pries BRG1 off the genomic DNA and prevents it from manipulating genetic activity."
He adds that when it comes to testing Myheart against heart failure in humans, the molecule itself is too large to be delivered as a drug.
Therefore, the team is now in the process of pinpointing smaller parts of the molecule that are crucial for blocking the BRG1 protein. If these subsections are found, the researchers say, they may end up with a compound that can be tested in human trials.
Medical News Today recently reported on a study by researchers from Abertay University in the UK, which detailed the creation of lab-grown mini beating human hearts that could offer a cure for heart disease.
Written by Honor Whiteman