In mammals, including humans, the ability of the heart muscle to recover after injury is very limited. After an acute myocardial infarction, millions of cardiomyocytes called cardiomyocytes die and are replaced by scars. Unlike mammals, other vertebrates can recover better from heart damage. This is the case with certain fish, including zebrafish, which is a recognized animal model in biomedical research and shares most of its genes with humans.
Zebrafish is very suitable for studying organ regeneration. After a heart injury, zebrafish cardiomyocytes can divide and the scar is replaced by a new heart muscle. Nadia Mercader's research group at the Institute of Anatomy at the University of Bern is interested in the cellular mechanisms of heart regeneration over the past decade. Now, researchers have shown that not all cardiomyocytes in the zebrafish heart make the same contribution to regenerating lost muscle, but there are specific subsets of cardiomyocytes that have enhanced regeneration capabilities.
"Repair Cells" expand more
Researchers cooperate with the interdisciplinary bioinformatics department of the University of Bern, EMBL (Heidelberg, Germany), CNIC (Madrid, Spain) and Universitario La Paz Hospital (Madrid, Spain). The study’s lead author Marcos Sande-Melón and his colleagues could use genetically modified tools to identify a small fraction of cardiomyocytes in the zebrafish heart characterized by the expression of the sox10 gene in response to injury Expand more than the rest of the cardiomyocytes. The gene expression profile of these cells is also different from the rest of the myocardium, indicating that they represent a specific subpopulation of cells. In addition, experimental removal of this small cell population will impair the regeneration of the heart. "We were able to identify specific cell populations that were more effective than all other cardiomyocytes in the regeneration process,
Possible correlation with human heart regeneration
Next, the author wants to figure out the role of sox10 in this cell population: "We want to find out whether the lack of sox10 cell population in mammals can explain why their hearts cannot regenerate well," Mercader explained. . If this is the case, the researchers believe that this discovery may be very important for stimulating the repair process of the human heart.