It may not be possible to fix a broken heart, but scientists have taken a new step towards healing the scars on one.

An international team of researchers has, for the first time, restored the elasticity in scarred heart tissue in rats by injecting them with a specific protein.

“What we have found is highly encouraging,” James Chong, a cardiologist, associate professor at the University of Sydney and senior author of the research, said in a press release.

“We hope to continue developing the method so it can eventually be used in a clinical setting and used to treat and improve the lives of the millions of heart failure patients worldwide.”

When a person experiences a heart attack, the actual tissue of the heart sustains trauma that becomes a scar – something that can cause problems down the line because scarred tissue isn’t able to stretch the way regular heart tissue can.

But according to the results of this new research, published last month in the peer-reviewed journal Circulation Research, we could be on the doorstep of a new way to reverse that damage.

In this preclinical study, researchers took a protein called tropoelastin – a spring-like molecule found in humans that aids in building elastic tissues – and injected it into rats in the days following a heart attack in an attempt to repair the scar tissue.

“Tropoelastin can repair the heart because it is a precise replica of the body’s natural elastic protein,” Anthony Weiss, co-author and professor with the Faculty of Science at the University of Sydney, said in the release.

In order to better ensure the success of the experiment, researchers also developed a new strategy of guiding the injection directly into the left ventricle of the heart with ultrasound, which is much less invasive than a thoracotomy, a surgical procedure to gain access to organs in the chest.

Around 28 days after injecting purified tropoelastin into the rats’ hearts, researchers observed that the heart muscle had regained its elasticity, and that its muscle function was similar to before the heart attack.

Researchers also found that the scar tissue had not expanded as much as in a control group of rats who were not treated with tropoelastin.

“This research showcases the potential of tropoelastin in heart repair and suggest further work will show exciting possibilities of its role in future treatments and therapies,” Dr. Robert Hume, lead researcher who is currently based at the University of Sydney`s Charles Perkins Centre, said in the release. 

Following a heart attack, dead cells are removed by the immune system in the first days. After three days, the body begins to replace those dead cells with scar tissue, which makes the heart less flexible and can increase the chance of further heart failure.

Heart disease, which can lead to a heart attack, heart failure or death, is the second leading cause of death in Canada.

The study also took the first steps to see if human cells reacted similarly to tropoelastin. Researchers treated a specific type of cardiac cells with tropoelastin in a petri dish and found that these isolated cells were able to generate the protein elastin after the treatment, suggesting injections of tropoelastin into human cells also has beneficial impacts.

We’re still a long way from testing out tropoelastin treatments on cardiac patients in a clinical setting. The study noted that further research is needed, as “an understanding into the exact mechanism behind tropoelastin ability to prevent scar expansion is not yet known.”

But if further studies with tropoelastin go well, researchers believe we could see larger animal preclinical studies and eventually human clinical trials. 

This content was originally published here.