(Philadelphia, PA) The stop and start of blood flow to the heart during and after a heart attack causes severe damage to heart cells, reducing their capacity to function and potentially causing their death. But a recent study led by researchers at Temple University School of Medicine suggests that it is possible to limit the extent of that damage using a drug. In experiments in mice that recapitulated a human clinical scenario, they discovered that inhibition of a heart protein called TNNI3K reduced damage from heart attack and protected the heart from further injury.
The findings have significant potential for translation into heart attack patients in a clinical setting. "Many times, what is done in a lab setting can't be done in patients," explained Ronald Vagnozzi, PhD, lead author on the new study, which appeared October 16 in Science Translational Medicine. "But we were interested in a real-world scenario."
Working with senior investigators Thomas L. Force, MD, Professor and Clinical Director at Temple University School of Medicine's (TUSM) Center for Translational Medicine, and Muniswamy Madesh, PhD, Assistant Professor in Temple's Department of Biochemistry, Cardiovascular Research Center, and Center for Translational Medicine, Vagnozzi created a real-world clinical scenario in mice by mimicking blockage of an artery to induce heart attack and then administering a TNNI3K inhibitor. When cardiac function was subsequently improved in treated mice versus untreated controls, Vagnozzi and colleagues realized that a TNNI3K inhibitor could have important clinical benefits for human patients.
"TNNI3K is found only in the heart, which makes it interesting biologically and therapeutically," Vagnozzi said. "Although its function was not well understood, TNNI3K lent itself to being a potential therapeutic target for heart attack."
The researchers found that TNNI3K expression is elevated in patients who are suffering from
|Contact: Jeremy Walter|
Temple University Health System