Mast cells as regulators of inflammation in heart failure

Cardiovascular diseases are the leading cause of death by non-infectious disease worldwide. Damage that occurs to the heart following a heart attack can lead to the formation of scar tissue in a process called fibrosis. Scar tissue in the heart interferes with its ability to pump, which drastically decreases the ability of the heart to function and ultimately leads to heart failure. As part of the Restitution Enhancement in Arthritis and Chronic Heart disease (REACH) team, I am working to determine what conditions promote or prevent fibrosis and heart failure. My research centres on an immune cell type called the mast cell, which is present in the human heart and is thought to be important in the development of fibrosis. However, the exact role of the mast cell in fibrosis is still not clear. Therefore, I hypothesize that mast cells respond to damage in the heart and promote proper healing without fibrosis. I will use samples obtained from human donors, as well as several animal models of disease, to analyze this question. This research will help us to gain a better understanding of the impact of the mast cell on the environment within the heart that could promote or inhibit heart failure. Through this work, we hope to identify potential targets for future drug development, or determine ways in which we can limit the development of fibrosis in future patients.