A protein that plays a key role in debilitating changes that occur in the heart after a heart attack has been identified by scientists.
A protein that plays a key role in debilitating changes that occur in the heart after a heart attack has been identified by scientists. These changes, or 'remodelling' of the heart, often lead to fatal heart failure.
Researchers found that mice genetically altered to lack fibronectin-EDA (FN-EDA) had less heart damage after a heart attack.
The findings hold potential for therapies to reduce or prevent heart muscle damage after a heart attack.
Researchers compared the effect of heart attacks in two groups of mice.
One group was genetically engineered to lack fibronectin-EDA (FN-EDA), a protein that exists in the space surrounding cells and is important for processes such as cell migration and wound healing. The other mice were genetically normal.
After inducing a heart attack in the left coronary artery of each mouse, the team found that the hearts of mice lacking FN-EDA had less enlargement in the left ventricle, better pumping ability and less thickening of the heart muscle) compared to the control mice.
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Bone marrow transplantation experiments revealed that the FN-EDA involved in the remodelling process came from the heart and not from cells circulating in the bloodstream.
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Source-ANI