Dr. Kraus’ research program currently consists of two components: The first is directed at a better understanding of cellular signaling pathways and mechanisms responsible for the adaptive responses of skeletal muscle to normal physiologic stimuli - such as exercise training - and to maladaptive responses to pathophysiologic stimuli -such as in congestive heart failure, skeletal muscle atrophy associated with chronic spaceflight and aging. We are using human studies, animal models and in vitro models of exercise to address these scientific questions. In this work, we have implicated signaling pathways involving cAMP in the responses of skeletal muscle to long term exercise training. We have found that gene expression in skeletal muscle in congestive heart failure is altered in a maladaptive fashion consistent with less effective exercise tolerance and long term disability associated with this condition. We have undertaken exercise training studies in human subjects designed to address questions about mechanisms of exercise training responses in skeletal muscle in normal subjects and those with chronic heart failure. Our in vitro models are designed to explore whether mechanical deformation of skeletal muscle cells (mechanotransduction) are responsible for some of the skeletal muscle responses to changes in contractile activity.
The second area involves human investigations of genetic susceptibility to complex cardiovascular conditions such as coronary artery disease and congestive heart failure. Our goals are several. First is to identify genetic markers that are associated with early onset cardiovascular disease and congestive heart failure so as to be able to better identify high risk subjects and those that may benefit from more aggressive preventive strategies. We also aim to identify causative genetic loci, so as to better understand the etiology and develop new therapeutic strategies for these conditions.
exercise, skeletal muscle, energy metabolism, cell signaling, gene expression, cell stretch, heart failure, aging, spaceflight, human genetics, early onset cardiovascular disease