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Breakthrough by Temple researchers could lead to new treatment for heart attack
Date:11/5/2013

heart failure, which can develop in the years following heart attack. To explore the significance of that elevation, they engineered mice to overexpress TNNI3K. They also created a second set of engineered mice, in which the protein was deleted. They then measured the animals' response to heart attack.

When overexpressed, Vagnozzi and colleagues found that TNNI3K promoted the injury of heart tissue from ischemia (blockage of blood flow) and reperfusion (restoration of blood flow) during and after a heart attack. TNNI3K overexpression in heart cells encouraged the production of superoxide, a reactive molecule from mitochondria, and activated p38 mitogen-activated protein kinase (MAPK), an enzyme that responds to stress signals in cells. The combined result of those activities was impaired mitochondrial function and heart cell death, which worsened ischemia/reperfusion injury. The opposite occurred in mice in which TNNI3K had been deletedsuperoxide production and p38 activation were reduced, and injury to the heart was limited. Reductions in heart dysfunction and fibrosis (hardening of heart tissue) were also observed.

The team next collaborated with the pharmaceutical company GlaxoSmithKline (GSK) to identify compounds that were capable of blocking TNNI3K activity. Treatment of wild-type (nonengineered) mice with the compounds following heart attack produced effects that were similar to those observed in mice with TNNI3K deletion.

The new findings open the way to a large-animal study and the development of a TNNI3K inhibitor that can be used in humans. According to Force, the team is planning to move ahead with a large-animal study, which will determine whether the drugs are effective in animals other than mice and allow for the development of pharmacological and safety profiles of the compounds. "Because TNNI3K is only expressed in the heart, drugs targeting it should be reasonably safe," Force noted.

A major aim of Temple's Ce
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Contact: Jeremy Walter
Jeremy.Walter@tuhs.temple.edu
215-707-7882
Temple University Health System
Source:Eurekalert

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