York University scientists have found that beta blockers could potentially protect against heart failure. The discovery is the latest in a field teeming with treatments that manage symptoms, but cannot reverse damage already sustained by the heart.
The team used mouse models of heart failure and next-generation sequencing to look at the RNA in heart cells. They pinpointed genetic changes in heart failure and studied what happened to these alterations when the mice were given beta blockers, a class of drugs commonly used to treat high blood pressure and some patients with heart conditions.
“We discovered that beta blockers largely reverse the pathological pattern of gene expression observed in heart failure,” said John McDermott, who led the research, in a statement. While more research is needed to grasp how individual genes function in the heart, McDermott said that reversing or blocking genetic changes could be “somehow protective” against heart failure. The work is published in Scientific Reports.
Heart failure, the inability of the heart to pump enough blood for the body’s needs, may be caused by several conditions, such as a heart attack or a birth defect.
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Physicians may prescribe their patients any combination of lifestyle changes, medical devices like implantable cardioverter defibrillators, or drugs, including beta blockers. While these treatments aim to preserve function, mortality is still high—about half of people who have heart failure will die within five years of diagnosis, the CDC said.
Many scientists are working on ways to stop the condition from getting worse, or to reverse it. Earlier this year, researchers at Nagoya University discovered that mice lacking a particular protein on the surface of heart cells were resistant to heart failure. Targeting this protein could result in a drug that prevents heart failure from worsening.
In a regenerative approach, a team from the University of Illinois at Chicago are taking skin cells, making them more like stem cells and then transforming them into blood vessels. When embedded in a gel and implanted into mice, these progenitor cells grew into human blood vessels, some of which connected to the mice’s own vessels and boosted heart function.
McDermott and his team at York University now plan to look into specific genes to see if they can be used in the diagnosis or treatment of heart failure.