IOWA CITY, Iowa, Dec. 8 (UPI) -- U.S. scientists say they've used a new mathematical model of heart cells to show how activation of an enzyme disrupts the electrical activity of heart cells.
Researchers from the University of Iowa and Columbia University say they've demonstrated the enzyme, calmodulin kinase II, is a critical regulator of the heart's response to injury.
"By targeting this enzyme's activity, it may be possible to prevent or treat heart disease and associated electrical rhythm disturbances," said University of Iowa researcher Thomas Hund, the study's senior author.
In the study, the team analyzed tissue from injured animal hearts in which a coronary artery had been blocked. They found a dramatic increase of levels of oxidized calmodulin kinase II in specific heart regions where potentially lethal electrical activity occurs.
Using the mathematical model of the cardiac cell, the researchers said they were able to predict the effects of oxidized CaM kinase on cardiac electrical activity.
"Oxidation appears to be a critical pathway for activation of CaM kinase in disease," Hund said. "Heart cells are very difficult to study, so improving our research tools -- as we did by creating the mathematical model -- is critical for generating new insight into heart disease mechanisms."
The research that included University of Iowa Associate Professor Peter Mohler and Professor Mark Anderson, as well as Columbia University Professor Penelope Bodyen, was published in the Dec. 3 online edition of the journal PLoS Computational Biology.
