A recent discovery may allow for direct treatment to prevent heart attacks.
In a study published in Nature in June 2015, researchers from the University of Virginia, Washington University in St. Louis, and the University of Pittsburgh found that smooth muscle cells (SMCs) are converted into macrophage-type cells in the presence of plaque and fat buildup, gaining the ability to fight infection. This transition is caused by Krüppel-like factor 4 (KLF4).
Heart attacks occur when cells in the heart die or are deprived of oxygen, usually due to a stoppage of blood flow to a certain part of the heart. Atherosclerosis, the buildup of plaque and fat in the inner walls of arteries, is a major cause of heart attacks, mostly due to inflammation of the tissue in response to the plaque (though the buildup of plaque and fat alone can also cause heart attacks).
When macrophages are present, they can often cause inflammation at sites where atherosclerosis has occurred, though they can also act as an anti-inflammatory. Researchers tested several methods of removing KLF4 – total removal lead to death after eight to ten weeks, but removal from certain cells resulted in a decrease in size and increased stability of the affected site. The results suggest that removing a single KLF4 gene globally could lead to a decrease in size, and increase in stability, of affected areas.
A letter in Nature last June, submitted by Michael Rosenfeld from the University of Washington’s Department of Pathology, noted this research suggests that it may be possible, with targeted drug treatment, to decrease artery blockage.
On average, every seven minutes someone in Canada has a heart attack, and over 16,000 of these attacks result in death, the Heart and Stroke Foundation estimates. Scientists are constantly working on new treatment options, and a new discoveries like this may allow for direct treatment to prevent heart attacks.
