Home News University of the Algarve research team make important cardiac disease discoveries

University of the Algarve research team make important cardiac disease discoveries

Published on 03/09/2019

The stem cell biology group of the University of the Algarve’s Centre for Biomedical Research (CBMR), led by José Bragança, has recently published a scientific paper that may bring “important conclusions” about the prevention of the onset of congenital heart disease in the journal Cell Death & Disease.

Among congenital diseases, “heart disease is the most common in humans (affecting about 1 in 100 babies),” says UAlg.

These heart diseases, which are present at birth, are a result of a failure in the development process of the embryo.

Several previous studies, including those by José Bragança, have shown that the CITED2 protein is critical for embryo survival and development and, in particular, for the cardiac development process to proceed normally.

This recent research, initially conducted with embryonic (mouse) stem cells, “provided a better understanding of the importance of the CITED2 protein in molecular mechanisms of cardiac differentiation, and led to the identification of proteins that may serve as supplements to compensate for the onset of cardiovascular abnormalities,” claimed the UAlg research team.

In these assays it was found that overproduction of the CITED2 protein leads to the secretion of two proteins – WNT5A and WNT11 – that have been shown to restore and promote heart development in the embryos of zebrafish with deficient CITED2 expression.

Thus, in this research, the scientists were also able to verify that the CITED2 protein plays a similar in both mice and humans, indicating that the function of the CITED2 protein is common in vertebrates from fish to humans.

“The results of this research are particularly important as they suggest that CITED2 dysfunction during development and perhaps other proteins may be offset by supplementation, opening the door for future clinical approaches to prevent or limit cardiac malformations during development without requiring gene therapies, ”concludes UAlg.