Burns Blaxall, PhD

Researchers report encouraging results in repairing scarred and poorly functioning heart tissues after cardiac injury.

In a study published online Aug. 14, 2017, in the Journal of the American College of Cardiology, researchers in our Heart Institute inhibited Gβγ and GRK2, proteins that regulate the heart’s response to adrenaline. This alleviated disease processes in mouse models of human heart failure, and in cardiac cells of patients undergoing reparative surgery.

After a heart attack, chronic overstimulation of the adrenaline system produces hypertrophy and fibrosis in the heart. Blocking Gβγ and GRK2 with the molecular inhibitor gallein preserved heart function and reduced enlargement and tissue scarring. Similar results were achieved when GRK2 was removed from cardiac fibroblasts in genetically altered mice.

The finding could revolutionize the treatment of heart failure, says senior investigator Burns Blaxall, PhD. Researchers are working on a compound that mimics gallein and is safe for use in animals and humans.