An immune cell that can nurse a heart back to health

Survival rates for heart attacks have dramatically improved over the years, and are now around 90%. That’s the good news. The bad news is that the resulting damage and inflammation to the heart is still the leading cause of heart failure. Dr. Matthew DeBerge is researching how a certain type of immune cell expels dead tissue from the heart and how it might be leveraged to restore its strength. View Halo Profile >>

Tell us about your research…

Acute myocardial infarction remains a leading cause of heart failure. Irreversible loss of cardiomyocytes from ischemia and subsequent reperfusion injury initiates a cascade of inflammatory events leading to adverse ventricular remodeling and loss of systolic function. Phagocytes within the heart, particularly macrophages, play an important role early after myocardial infarction to determine the extent of inflammation and set the clinical trajectory for disease progression.

My research focuses on the balance of inflammatory and reparative responses by examining the mechanisms regulating macrophage clearance of apoptotic cells (efferocytosis) and how this directs the anti-inflammatory macrophage response after myocardial infarction.

Can you explain that to a non-scientist?

Following a heart attack, increased inflammation is linked to poor outcomes. Immune cells within the heart play important roles in the response to a heart attack by controlling the levels of inflammation. My research investigates how cells of the immune system promote clearance of dead tissue to drive heart repair and limit excessive inflammation after a heart attack.

My research investigates how cells of the immune system promote clearance of dead tissue to drive heart repair and limit excessive inflammation after a heart attack.

How could it someday impact patient lives?

A precise understanding of inflammatory and reparative responses by macrophages after myocardial infarction would provide valuable insight towards the generation of therapeutic targets to reduce inflammation and adverse tissue remodeling and limit progression to heart failure.

In addition to the importance of these studies to heart failure, the mechanisms are likely translatable to other cardiovascular and ischemic diseases, such as diabetic wounds or stroke.

In addition to the importance of these studies to heart failure, the mechanisms are likely translatable to other cardiovascular and ischemic diseases, such as diabetic wounds or stroke.