My lab focuses on studying why heart function declines as we age. Older people have significantly higher rates of cardiovascular disease, including heart attack, stroke, and heart failure, compared to younger individuals. But also, elderly people with no overt cardiovascular disease still exhibit declines in cardiac function, which can lead to exercise intolerance and a cascade of other negative consequences.
Why does this happen? We are using mouse models to study these processes, because the aging mouse heart closely represents what happens in a human heart with age.
We know that cardiac function, both contraction and relaxation of the heart, is impaired with aging. But the deficit in relaxation is more significant than contraction, and we want to investigate the mechanisms behind this age-related impairment in relaxation. When the heart doesn’t relax as it should, it doesn’t completely fill. This reduces cardiac output and ultimately contributes to compromised heart function.
In my lab, we study how cellular and molecular changes during natural aging affect cardiac function, especially cardiac relaxation properties. By understanding the mechanisms of how aging impairs heart function, we can look for potential drugs or interventions targeting these mechanisms to improve cardiac function in the elderly. Our goal is to develop drugs or interventions to delay, lessen or even reverse some of the negative changes in the heart that are caused by natural aging.