Heart disease—the nation’s leading cause of death—is responsible for one in every four deaths in the U.S. These chilling statistics motivate one researcher’s interest in heart muscle cells, the hard-working cells that keep the blood pumping through our bodies.
Zhaokang Cheng, Ph.D., an assistant professor in the College of Pharmacy, studies the molecular processes that cause cell death in heart muscle cells. When heart muscle cells die, the body does not regenerate new cells. As a result, the surviving cells have to work harder to keep the heart going. Depending on the extent of heart damage, this may result in a weakened heart or even heart failure. That’s why it’s important to find ways to protect heart muscle cells from conditions that damage them, including heart attacks and toxicity caused by certain chemotherapy (anti-cancer) drugs.
With funding from a five-year NIH grant, Cheng is working to understand the mechanisms that underlie heart muscle cell death after exposure to doxorubicin, a commonly used chemotherapy drug.
“Doxorubicin is very effective at controlling tumor growth, but when used in large cumulative doses it can, over time, lead to heart disease,” Cheng said. As part of his study, he is trying to identify what genes and proteins may be involved in heart muscle cell death in response to doxorubicin toxicity.
“Once we understand how these cells die, we can use that knowledge to try to develop a heart-protective drug to increase long-term survival in cancer patients and improve outcomes following a heart attack,” said Cheng.
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