Insulin-mediated ROS/RNS signaling in cardiac myocytes

In Austria, a person dies every fifty minutes as a consequence of diabetes mellitus. First described in the 16th century, this metabolic disorder has been one of the most common prosperity diseases since the 1960s. Pathologically increased blood glucose levels interfere with many cell functions, causing faster aging and various secondary diseases. Diabetes is associated with multiple consecutive symptoms which cause high therapy costs, notably neurological disorders and cardiovascular diseases. People suffering from diabetes frequently develop typical pathologies, generally termed cardiomyopathy and featuring prominently among the most frequent causes of death. However, the molecular changes triggering these typical syndromes are largely unknown. In this research project conducted in cooperation with Prof. Thomas Michel of the Harvard Medical School in Boston (USA), we are investigating specific signal changes resulting in functional disorders in diabetic cardiomyopathy. To this end, we use sophisticated biosensors which we have recently developed in our laboratory. These novel probes and powerful microscopy techniques enable real-time imaging of reactive oxygen and nitrogen species in cardiac muscle cells. Radicals like hydrogen peroxide or nitric oxide are small molecules which, when in excess, can prove harmful. We assume that insulin, the very hormone whose blood-glucose-level-inhibiting function is impaired in diabetics, triggers excessive formation of such radicals in the diabetic heart, thus disrupting the physiological function of the myocardium. Insights gained from this research can lead to the development of improved therapeutic avenues.

No additional funding sources recorded.