We are pursuing research on the biochemical and molecular basis of longevity regulation to provide novel therapeutic options to prevent and cure age-related diseases like obesity, diabetes, neurodegeneration and cancer.
We are interested in genetic pathways and environmental factors that modulate longevity. Besides other topics, we are particularly focused on the role played by mitochondria in lifespan regulation. In the past and contrary to the widely reiterated Free Radical Theory of Aging, we have repeatedly shown that the health-promoting effects associated with low caloric intake, physical exercise, sirtuins, impaired insulin/IGF-1 signaling, and other lifespan-extending interventions may be due to increased formation of Reactive Oxygen Species (ROS) within the mitochondria, causing a vaccination-like adaptive response that culminates in increased stress resistance and extended longevity, a process a. k. a. mitochondrial hormesis or mitohormesis.
Based on this and meanwhile, we characterize identify and aging-associated pathways that have been identified by a RNA expression screen of physiological aging in several evolutionary distinct species, including C. elegans, zebrafish, killifish, and mice.