Researchers have discovered a previously unidentified cell population with the power to heal injured hearts. The cells were found in the pericardial fluid inside the sac around the heart.
Gata6+ pericardial cavity macrophage
The study was led by Drs. Paul Kubes, PhD, Justin Deniset, PhD and Paul Fedak, MD, PhD. The specific cell is called a Gata6+ pericardial cavity macrophage. In mice, it has been found to help heal injured hearts.
The same cells were also found within the human pericardium of people with injured hearts. The researchers believe this confirms that the repair cells may provide new therapies for patients with heart disease.
The heart is known for its very limited capacity to repair itself making heart disease the number one cause of death in North America. This is the first time that heart doctors explore the possibility that cells outside the heart could participate in the healing and repair of hearts post injury.
"Our discovery of a new cell that can help heal injured heart muscle will open the door to new therapies and hope for the millions of people who suffer from heart disease. We always knew that the heart sits inside a sac filled with a strange fluid. Now we know that this pericardial fluid is rich with healing cells. These cells may hold the secret to repair and regeneration of new heart muscle. The possibilities for further discovery and innovative new therapies are exciting and important," said Fedak, a professor in the Department of Cardiac Sciences.
Impressively, the researchers have identified the cell in less than three years, a quick time frame to move from the lab and animal models to people. Now, they hope to move the research to a broader study of human heart repair.
The new program will seek out potential new therapeutics to improve heart repair. The research is supported by the Heart and Stroke Foundation of Canada, the Canadian Institutes of Health Research, the Canada Research Chairs Program, and the National Institutes of Health.
The study is published in the journal Immunity.