By means of a novel mathematical model of heart cells, researchers from the University of Iowa have apparently demonstrated as to how activation of a vital enzyme, calmodulin kinase II (CaM kinase), could disturb the electrical activity of heart cells.
In this research, the team apparently examined the tissues from the damaged hearts of animals in which a coronary artery had apparently been obstructed. They supposedly discovered a drastic escalation in the levels of oxidized CaM kinase in particular heart areas where potentially fatal electrical movement supposedly takes place.
Thomas Hund, Ph.D., associate in internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine and the paper’s senior author, commented, “Recently, researchers have developed great interest in calmodulin kinase II as 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.”
He added, “CaM kinase is activated when the heart experiences injury, for example, when an artery providing blood to the heart becomes blocked. In the short-term, this increase in activity may be the heart’s attempt to increase blood flow. However, unfortunately, the initial response results in a vicious cycle that likely advances heart disease.”
By means of the mathematical model of the cardiac cell, the researchers could envisage through computer simulation, the supposed outcomes of oxidized CaM kinase on cardiac electrical activity.
Oxidation apparently generates the enzyme by altering chief chemical groups. In heart disease, oxidation is said to be overactive, and CaM kinase is supposedly switched on in excess.
Hund remarked, “Oxidation appears to be a critical pathway for activation of CaM kinase in disease.”
Hund concluded by mentioning that heart cells are very difficult to study, so improving their research tools, as they did by creating the mathematical model, is critical for generating new insight into heart disease mechanisms.
The research was published in the journal PLoS Computation Biology.