Pointing to a new direction of drug development, a new research by the Peter Munk Cardiac Centre has found that switching of a protein can be a cause of 'a cascade of events' leading to heart failure.
"Our research suggests that PINK1 is an important switch that sets off a cascade of events affecting heart cell metabolism. This could be one of the inciting events in the development of heart failure," said Dr. Phyllis Billia, principal author, clinician-scientist and heart failure specialist at the Peter Munk Cardiac Centre.
The findings show that the absence of a certain protein, PINK1, causes some heart cells to die, forcing the remaining cells to work harder to keep the heart going. In response to this stress, the heart muscle cells thicken, a condition known as hypertrophy.
"The discovery of PINK-1's role in the development of heart failure may lead to novel treatment to prevent heart failure in those at risk. This discovery represents a novel and as yet, untapped mechanism to fight the battle against heart failure," said Dr. Vivek Rao, co-author of the study and Surgical Director of the Heart Transplant Program at the Peter Munk Cardiac Centre.
In the lab, researchers genetically removed the PINK1 gene in mice and studied their heart cells under the microscope. They found that though PINK1 is not required for organ development, it is crucial to prevent heart failure.
The findings were published in Proceedings of the National Academy of Sciences.