Stanford University researchers have created a protein patch that they said would repair heart attack damage. According to a report by Medical News Today, the patch has worked on animal testing when damages on mouse and pig hearts caused by heart attack were reversed by the patch. The patch is said to be available for human clinical trials by 2017.
Each year around 735,000 people in the U.S. have a heart attack. Heart disease claims the lives of 610,000 Americans annually. Around 124,000 people in the UK suffer a heart attack each year.
During a heart attack, muscle cells in the heart die because of lack of oxygen due to reduced blood flow. The damaged heart tissue isn’t easily repaired which may turn into awful scar tissue. Scientists believe that these tissues need to be repaired in order to avoid long-term damage.
There is no treatment available to repair the heart tissue damage. These damaged tissues may lead to abnormal heart beat or even heart failure.
The lead researcher of the study Prof. Ruiz-Lozano and his team focused on developing a treatment that would explain why the cardiomyocytes fail to regenerate.
The researchers studied zebrafish which regenerates its own heart cells using the epicardium that releases more than 300 proteins that activate the replication of the cardiomyocytes.
The team identified a protein called Follistatin-like 1 (FSTL1) in the epicardial tissue that prompted the replication of the cardiomyocytes. In humans, this protein diminishes after a heart attack and that is why damaged heart cells are not easily repaired.
The researchers then created a patch made of acellular collagen and soaked it in the protein FSTL1. Then they attached it to the damaged hearts of pigs and mice that had experienced heart attacks. After two weeks, heart function in these animals improved and it triggered the replication of existing muscle cells which grew new blood vessels.
Prof. Ruiz-Lozano believes that prior to receiving the patch, many of the animals were very sick and would need a heart transplantation. He hopes that the new findings will break the ground for a completely revolutionary treatment for heart disease.
Mark Mercola, a co-author of the study and a professor bioengineering at UCSD described the patch as “clinically viable and “clinically attractive.” Because the patch does not contain any cells, there would be no need for an immunosuppressive medication.
The researchers concluded by saying:
“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 remodeling following myocardial infarction in humans.”
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