Heartening Protein Patch Developed to Repair Cardiomyocyte Damage

A REVOLUTIONARY ‘protein patch’ has been developed that repairs the damage caused by a heart attack. Investigating a treatment to address the inability of heart muscle cells to regenerate, researchers found that the patch improved overall heart function and survival of the test subjects. The team hopes that these findings will pave the way for a pioneering treatment for heart attack patients.

During a heart attack or myocardial infarction, reduced blood flow causes a lack of oxygen that leads heart muscle cells – known as cardiomyocytes – to suffer damage and die. Cardiomyocytes in adult mammals are subsequently unable to fully regenerate, which means that the heart muscle forms scar tissue in an attempt to heal. This heart damage, which is currently untreatable, can lead to arrhythmias, heart failure, and other complications.

The study, led by Prof Pilar Ruiz-Lozano, Associate Professor (Research) of Pediatrics (Cardiology), Stanford University, Stanford, California, USA, aimed to develop a treatment to address this issue. The team used mass spectrometry to analyse more than 300 proteins produced by epicardial cells, as these are known in zebra fish to regenerate cardiomyocytes. Of these proteins, they eventually identified one called Follistatin-like 1 (FSTL1) that stimulates cardiomyocytes to replicate. Embedding this protein into an acellular collagen patch, they tested it on the hearts of pigs and mice that had been damaged by heart attack.

The team found that the patch began to trigger growth of new blood vessels and regeneration of existing cardiomyocytes within 2–4 weeks. Both the overall heart function and the survival of the animals improved, even when the patch was applied only a week after heart attack.

“The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans,” concluded the authors, who state that the patch is both clinically viable and clinically attractive. Furthermore, the authors have expressed that a patient would not need to use immunosuppressive medication, as the patch is acellular; they hope that human clinical trials for the patch will be able to start in the next 2 years.

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