Heart attack repair kitby Leigh MacMillan Aug. 16, 2011, 8:00 AM
Myocardial infarction is the leading cause of death worldwide. Because current therapies do not repair damaged cardiac tissue, MI often leads to heart failure – an inability of the heart to meet the body’s blood flow needs.
Previous studies have suggested that the Wnt signaling pathway, a network of proteins with roles in development, cancer and normal physiological processes, could be a therapeutic target to improve heart muscle repair after MI, but the results have been contradictory. To clarify the Wnt pathway’s role, Antonis Hatzopoulos, associate professor of cell and developmental biology, and colleagues examined Wnt signaling after an experimental MI in mouse models. They report in the July issue of Disease Models & Mechanisms that a large number of Wnt-positive cells accumulate in the infarct area one week after MI. They also showed that MI triggers a cellular change called endothelial-to-mesenchymal transition (EndMT), and that Wnt signaling is active in EndMT-derived mesenchymal cells that take part in cardiac tissue repair after MI.
The findings could lead to new strategies to improve cardiac repair through manipulation of the Wnt signaling pathway.