Opening a blocked coronary artery to restore blood flow to the heart prevents sudden cardiac death. However, doing so also triggers cardiac damage through oxidative stress and inflammation, which eventually can lead to heart failure. In a new study, researchers at the University of Missouri School of Medicine have identified a protein that can be targeted to decrease post-heart attack injury and prevent heart failure in a mouse model.
“Heart attacks are one of the most common causes of death and disability worldwide,” said Chandrasekar Bysani, D.V.M., Ph.D., Margaret Proctor Mulligan Endowed Professor of Medicine at the MU School of Medicine and lead author of the study. “Treating a heart attack involves opening a blocked coronary artery. However, the natural inflammatory process that results from opening the blockage also causes short- and long-term damage to the heart. Currently, there are no treatments that address this issue. Our study found a way to minimize this inflammation by reducing levels of a protein called TRAF3IP2.”
Bysani, who also serves as a research career scientist at the Harry S. Truman Memorial Veterans’ Hospital, found in previous research that TRAF3IP2 helps initiate cardiovascular inflammatory responses. Using ultrasound technology, Bysani’s research team delivered a protein inhibitor directly to the hearts of mice to decrease production of TRAF3IP2.
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