A team from the School of Medicine at Stanford University (USA) has found a protein capable of inducing the regeneration of heart cells after a heart attack in mammals, according to a study published in Nature.
The Spanish group led by Pilar Ruiz-Lozano has investigated the role of protein in the heart FSTL1 system of mice and pigs, whose heart, like that of other mammals, has limited ability to repair itself after a substantial loss of cells muscle (cardiomyocytes).
Scientists have identified that protein often found in the lining of the walls of a healthy heart (epicardium), but disappears in that area after a heart attack.
This situation can be reversed, however, applying a patch that simulates tissue epicardium and acts as a source of FSTL1 protein, which is achieved trigger proliferation of cardiomyocytes and cardiac function is improved.
“My team has patented a technology that we hope to market clinical applications” of this discovery, said the study’s lead author.
The future human therapy to counteract the effects of a heart attack would be to install a patch by surgery after a heart attack.
45% of heart muscle cells are renewed throughout the life of a human being, while 55% remain unchanged from birth.
That regeneration rate is not enough to repair the damage caused by a heart attack, so, after suffering the trauma, the body covers the affected area of heart tissue fibroblasts, cells with little ability to contract to the Long compromise the organ’s ability to pump blood.
So far, the bulk of the investigation to a regenerative therapy has focused on the use of immature muscle cells derived from stem cells.
The Ruiz-Lozano group opted instead to investigate the characteristics of the FSTL1 protein, which previous studies had already revealed as a precursor to the development of various organs.
This protein plays a role in a wide range of diseases, such as arthritis, pulmonary fibrosis and cancer, due to their ability to activate cellular communication mechanisms.
Depending on which organ is, the protein is able to cause inflammatory responses, act as a factor of protection or induce cellular immune responses.