Debilitating changes that occur in the heart after a heart attack may now be reduced, thanks to the following discovery. A team of experts asserts that the protein fibronectin-EDA (FN-EDA) can be targeted to reduce damage after heart attack. The research findings can possibly aid on designing future therapies for preventing or reducing heart muscle damage after a heart attack.
At the time of the investigation, two groups of mice were compared to analyze the effect of heart attacks. While one group was genetically engineered to lack the protein, other mice were genetically normal. The protein FN-EDA presumably exists in the space surrounding cells and is important for processes like migration and wound healing. On inducing a heart attack in the left coronary artery of each mouse, scientists found that the hearts of mice lacking FN-EDA allegedly had fewer enlargements in the left ventricle.
These mice also reported better pumping ability and less thickening of the heart muscle than the control mice. When genetically engineered mice were examined at the tissue level, it was pointed out that these mice supposedly had less inflammation, diminished activity of the enzymes metalloproteinase 2 and 9, which are involved in heart remodeling and declined myofibroblast transdifferentiation. After conducting bone marrow transplantation experiments it was ascertained that the FN-EDA involved in the remodeling process comes from the heart and not from cells circulating in the bloodstream.
The research is published in Circulation Research: Journal of the American Heart Association.