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health. Furthermore, the recommendations have not been tested in any study before being applied. The results indicated that cardiac cells that had the GATA4 mutation showed alterations when compared to reprogrammed cells from people without the abnormality. Specifically, the presence of the mutation caused structural defects and modifications in the metabolic activity of the cells, which also did not contract properly. Additionally, the authors showed that the G296S mutation in GATA4 prevents the recruitment of the isino factor TBX5 to regions of the genome responsible for increasing the expression of specific genes in cardiac tissue. This phenomenon affects the expression pattern of components of a gene network necessary for normal development of the heart and muscle contraction. On the other hand, the absence of TBX5 in these regions induces changes in chromatin that favor the expression of endothelial genes that should be repressed.
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