In its latest research, a team of health and bioengineering experts discovered that a protein can promote heart muscle healing in select animals that have suffered a heart attack.

While human hearts cannot repair themselves after they are damaged, the hearts of other species seem able to. Fish, for instance, can regenerate cardiac muscle. Inspired by this, the team led by Stanford University's Professor Pilar Ruiz-Lozano decided to test these species' heart cells and determine which compounds stimulate the healing. They were able to discover that the compound was FSTL1, a protein that stimulated cardiac muscle cell division.

They then made collagen patches of FSTL1, and samples of these patches were then used on mouse and pig hearts subjected to experimental heart attack. The team was excited to find that the FSTL1 was able to facilitate cellular rebuilding in the heart to repair the damage, even if the patch was implanted after the attack. In one pig, left ventricular function improved from 30 to 40 percent after patch application even when it was used a week after the injury. Heart muscle scarring was also considerably less.

Heart attacks occur when a blood vessel supplying the heart is blocked either by cholesterol or a clot, causing cellular death and failure to function. Thanks to modern medicine, patients who have sustained cardiac damage can survive and live longer under constant medication and monitoring. However, because there is no current modality available to promote cardiac muscle healing and reduce scarring, heart attack survivors can die within five to six years due to eventual heart failure.

Ruiz-Lozano believes this could be a breakthrough, since facilitating the healing of heart muscles can decrease its chances of further breakdown and also improve overall functioning.

"Treatments don't deal with this fundamental problem—and consequently many patients progressively lose heart function, leading to long-term disability and eventually death," Ruiz-Lozano said.

Other team members shared her excitement, saying that, if proven successful in human trials, the treatment is the key to many possibilities.

"We are really excited about the prospect of bringing this technology to the clinic," Mark Mercola, professor of bioengineering at University of California San Diego, said. "It's commercially viable, clinically attractive and you don't need immunosuppressive drugs." Because of the success of the experiment, researchers are hoping that human clinical trials can be carried out by 2017.