Heart Attack-Related Scarring Could Be Treated With New Protein Patch That Stimulates Tissue Regeneration

Scientists have identified a protein that helps heart muscle cells regenerate following a heart attack, and a patch packed full of these proteins and placed directly on the heart was shown to greatly improve cardiac function and survival rates in both mice and pigs.

The researchers believe the protein patch could be tested in humans as soon as the year 2017, the University of California, San Diego reported. Animal models that suffered heart attacks and were treated with the patch regained close to normal function within four to eight weeks.

"We are really excited about the prospect of bringing this technology to the clinic," said Mark Mercola, professor of Bioengineering at UC San Diego and professor in the Development, Aging, and Regeneration Program at SBP. "It's commercially viable, clinically attractive and you don't need immunosuppressive drugs."

The protein Follistatin-like 1 (FSTL1) was found to stimulate cultured heart cell muscles to divide. In animal models that had undergone an experimental form of myocardial infarction, a patch that applied these proteins proved to rebuild the damaged heart tissue and reduce scarring, two factors that current heart attack treatments fail to address.

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

Scarring associated with a heart attack can make it more difficult for the heart to pump blood, which can eventually lead to heart failure; about half of heart failure patients die within five to six years. Current heart attack treatments can make it easier for the heart to pump blood, but do not have the ability to regenerate heart tissue.

To make their findings, the researchers looked at the way fish naturally regenerate heart tissue by producing regenerative compounds in the heart's outer layer. By looking at epicardial cells, the team demonstrated that they stimulated existing heart muscle cells to replicate. They identified the protein responsible for this phenomenon using mass spectrometry and high throughput assays. Using this information, the researchers created a therapeutic patch made out of collagen that was cast with FSTL1.

"It could act like a cell nursery," Ruiz-Lozano said. "It's a hospitable environment. Over time, it gets remodeled and becomes vascularized as new muscle cells come in."

The findings were published in a recent edition of the journal Nature.

Tags
University of California, San diego, Nature, Heart disease, Cardiovascular Disease, Stanford university
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