The findings, published in the April issue of Nature Medicine, suggest that medicines designed to block CaM kinase activity may be useful for treating patients with structural heart disease and myocardial dysfunction.
Heart disease remains the number one killer in the United States. Most of that disease is in individuals who have suffered a heart attack or who have had changes in the heart muscle, including hypertrophy and dilation, for other reasons, said Mark E. Anderson, M.D., Ph.D. Betty and Jack Bailey Professor of Cardiovascular Medicine at Vanderbilt and the senior investigator of the current study.
"People with structural heart disease die suddenly from electrical instability arrhythmias and also because the heart fails to function properly as a pump," said Anderson, who is also associate professor of Medicine and Pharmacology.
Anderson and Roger J. Colbran, Ph.D., associate professor of Molecular Physiology & Biophysics at Vanderbilt University Medical Center, have collaborated for a number of years to study the role of the protein CaM kinase in signaling pathways that underlie the heart's electrical stability and maintenance of normal rhythm. Several years ago, they demonstrated in a mouse model of cardiac hypertrophy that blocking CaM kinase activity suppresses arrhythmias.
At the same time, evidence from other laboratories began to suggest that CaM kinase's role in structural heart disease went beyond the electrical signaling network. CaM kinase protein was consistently elevated in patients and animals with structural heart disease. And mouse lines genetically engineered to produce excess
Contact: Clinton Colmenares
Vanderbilt University Medical Center