Delivering Missing Protein Heals Damaged Hearts in Animals
But by placing a bioengineered patch that mimics membrane tissue and acts as a source of FSTL1 on damaged mouse and pig hearts, the study authors found heart muscle cells started growing and spreading, improving heart function and survival. The new creation could be set to enter human clinical trials as early as 2017.
Two weeks later the hearts began to grow fresh muscle cells and new blood vessels, while showing signs of pumping more effectively.
There is now no effective treatment to reverse the scarring in the heart after heart attacks.
Many people survive heart attacks, the event usually leaves lasting damage to muscle and tissue within the heart.
The results were remarkable – the protein not only reduced scarring, but it rebuilt the damaged heart as well.
Furthermore, the patches contained no cells, but were specifically made of the main structural protein in the extracellular space named “collagen”.
A group of researchers managed to embed a naturally-occurring protein into a patch which can help heal muscles damaged by heart attacks.
Writing in the journal Nature, researchers say the patch may one day revolutionise treatment.
The heart rate of a pig which suffered from heart attack dropped from 50% to 30% in the left ventricle. They then designed a collagen-based material coated in FSTL1, and placed it on the hearts of pigs and mice forced to have a heart attack. This would change future treatment, and lead to the reduction of long-term damage in the event of a heart attack. “We are really excited about the prospect of bringing this technology to the clinic”, said Mark Mercola, Ph.D., professor in the development, aging, and regeneration program at SBP and professor of bioengineering at UC San Diego. These cells led to less scarring, and the animal’s hearts returned to near normal function very soon after the procedure.
The protein in question is called Follistatin-like 1 (FSTL1), and initial tests in lab environment showed that the protein can stimulate cultured heart muscle cells to divide. He adds, “It’s commercially viable, clinically attractive and you don’t need immunosuppressive drugs”.
Scientists at the Stanford University School of Medicine and their colleagues from the University of California-San Diego have delivered a protein to hearts damaged by heart attacks that helps injured tissue regenerate. Eventually sustained pressure causes the scarring to spread to nearby areas and causes heart failure.