Heart failure is a condition in which the heart muscle becomes very weak. It is most often the result of multiple genetic disorders and coronary artery disease, in which plaque builds up inside the arteries, reducing blood flow and "starving" the heart muscle. As a result, the heart is unable to pump enough oxygen and nutrients to vital organs throughout the body.
Dr. Akhter believes that the protein kinase C--a molecule activated when the heart becomes enlarged--"turns on" a specific enzyme that limits the heart's ability to respond to stress and pump efficiently. This can lead to poor heart function and, ultimately, heart failure.
He and his team will study the interaction between these two signaling molecules in multiple lines of genetically engineered mice--each designed to express a specific kinase or kinase inhibitor--in order to identify new ways to prevent heart function deterioration.
"If we can identify and block this molecular 'cross-talk' that contributes to heart failure, we can develop new, more precise therapies that reduce the incidence of disease and save more lives," Dr. Akhter says.